ABSTRACT
Objective:To explore the effect of intravenous thrombolysis in patients with acute ST segment elevation myocardial infarction (STEAMI) caused by acute occlusion of venous bridging vessels.Methods:The clinical data of a patient with acute STEMI caused by acute occlusion of venous bridge in the North China University of Science and Technology Affiliated Hospital in 2019 was retrospectively analyzed.A 58-year-old male patient underwent coronary artery bypass grafting (CABG) 12 years ago.He was re-admitted to the hospital due to acute inferior ST-segment elevation myocardial infarction for 4 hours.He was given Immediately aspirin 0.3 g chewed, ticagrelor 180 mg orally, heparin 4000 U intravenous injection.Next, he was given 50 mg of recombinant prourokinase intravenous thrombolysis.The successful thrombolysis was judged by observing the relief of chest pain symptoms, the ST segment of ECG falling down and the moving of myocardial enzyme peak.Coronary angiography was performed to observe the pathological changes of coronary artery and Bridge in situ, and further treatment strategies were formulated.Cardiac ultrasound examination was performed to understand the structure and function of the heart.The patients were followed up for 1 year to observe whether there were angina pectoris and cardiovascular events.Results:Thrombolytic therapy was successful at 1 hour.Coronary angiography was performed on the 8th day after acute inferior STEMI.The culprit vessel was ascending aorta great saphenous vein right coronary artery.The whole course was diffuse lesions with a large number of thrombus shadows.In situ, the left main coronary artery was diffuse 60% stenosis, the ostia of anterior descending branch and right coronary artery were completely occluded, and the proximal part of circumflex artery was completely occluded.The patients were given intensive antithrombotic therapy for 14 days, and he got better and was discharged.On the 41st day after acute STEMI, coronary angiography was reexamined.Thrombus shadow in aorta great saphenous vein right coronary artery disappeared.Echocardiography showed that left ventricular diastolic diameter was 53 mm and ejection fraction was 55%.The patient was given improved lifestyle and intensive drug treatment.One year after myocardial infarction, the patient had no angina pectoris and was competent for daily work and life.Conclusion:For patients more than 10 years after CABG, with chronic occlusion of coronary artery in situ, when acute STEMI caused by venous bridge occlusion, intravenous thrombolytic therapy is in line with the principle of early reperfusion treatment and has a good prognosis.
ABSTRACT
<p><b>OBJECTIVE</b>To investigate the effects of spironolactone on the concentration of collagen type I, III in the myocardium of spontaneous hypertension rats (SHR).</p><p><b>METHODS</b>Twenty 8-week male SHR were assigned randomly into spironolactone (SHR-SPIRO, n=10) and control groups (SHR-CON, n=10), sex-age matched Wistar Kyoto rats (WKY group, n=7) were also served as controls. The rats of SHR-SPIRO group were given 20 mg/(kg*d) of spironolactone, the rats of SHR-CON and WKY groups were given the same volume of distilled water. After 16 weeks, the concentration of collagen type I was analyzed with Western blot. The areas of collagen type I and III were observed under polarized light microscopy and the ratio of type I/III collagen was calculated through accumulation score.</p><p><b>RESULTS</b>Compared with WKY group,the concentration of collagen type I in SHR-CON group was significantly higher (1.87 ±0.2 Compared with 1.21 ±0.7, P<0.05). After 16 weeks of treatment the concentration of collagen type I (1.42 ±0.05 Compared with 1.87 ±0.2, P<0.05) and I/III ratio in SHR-SPIRO group were significantly reduced (15.64 ±1.34 Compared with 20.8 ±3.04, P<0.05) compared with SHR-CON group; but there were no differences in accumulation area scores of collagen type III among three groups (368.3 ±30.2 Compared with 481.6 ±32.4 Compared with 406.2 ±45.3, P>0.05).</p><p><b>CONCLUSION</b>The deposition of collagen type I in myocardium may be involved in myocardial fibrosis of SHR, and spironolactone can decrease the concentration of collagen type I, which may be one of the mechanisms for its therapeutic effects.</p>