Treatment of myocardial infarction (MI) remains a major challenge. The chemokine family plays an important role in cardiac injury, repair, and remodeling following MI, while stromal cell‐derived factor‐1 alpha (SDF‐1α) is the most promising therapeutic target. This study aimed to increase SDF‐1α expression using a novel gene delivery system and further explore its effect on MI treatment. In this study, two kinds of plasmids, human SDF‐1α plasmid (phSDF‐1α) and human SDF‐1α‐ nuclear factor κB plasmid (phSDF‐1α‐NFκB), were constructed and loaded onto cationic microbubble carriers, and the plasmids were released into MI rabbits by ultrasound‐targeted microbubble destruction. The transfection efficiency of SDF‐1α and the degree of heart repair were further explored and compared. In the MI rabbit models, transfection with phSDF‐1α‐NFκB resulted in higher SDF‐1α expression in peri‐infarct area compared with transfection with phSDF‐1α or no transfection. Upregulation of SDF‐1α was shown beneficial to these MI rabbit models, as demonstrated with better recovery of cardiac function, greater perfusion of the myocardium, more neovascularization, smaller infarction size and thicker infarct wall 1 month after treatment. Ultrasound‐targeted cationic microbubbles combined with the NFκB binding motif could increase SDF‐1α gene transfection, which would play a protective role after MI.

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BACKGROUND As an established, simple, inexpensive, and surprisingly effective diagnostic tool, right-heart contrast echocardiography (RHCE) might help in solving a vexing diagnostic problem. If performed appropriately and interpreted logically, RHCE allows for differentiation of various usual and unusual right-to-left shunts based on the site of injection and the sequence of microbubble appearance in the heart. CASE SUMMARY A 31-year-old woman was readmitted to hospital with a 2-mo history of worsening palpitation and chest distress. Two years prior, she had been diagnosed with postpartum pulmonary embolism by conventional echocardiography and computed tomography angiography. While the latter showed no sign of pulmonary artery embolism, the former showed pulmonary artery hypertension, moderate insufficiency, and mild stenosis of the aortic valve. RHCE showed microbubbles appearing in the left ventricle, slightly delayed after right-heart filling with microbubbles; no microbubbles appeared in the left atrium and microbubbles’ appearance in the descending aorta occurred nearly simultaneous to right pulmonary artery filling with microbubbles. Conventional echocardiography was re-performed, and an arterial horizontal bidirectional shunt was found according to Doppler enhancement effects caused by microbubbles. The original computed tomography angiography findings were reviewed and found to show a patent ductus arteriosus. CONCLUSION RHCE shows a special imaging sequence for unexplained pulmonary artery hypertension with aortic valve insufficiency and simultaneous patent ductus arteriosus.