RESUMO
BACKGROUND: The combination of acute ST-segment elevation myocardial infarction (STEMI) and gastric ulcers poses a challenge to primary percutaneous coronary intervention (PPCI), particularly for young patients. The role of drug-coated balloons (DCBs) in the treatment of de novo coronary artery lesions in large vessels remains unclear, especially for patients with STEMI. Our strategy is to implement drug balloon angioplasty following the intracoronary administration of low-dose prourokinase and adequate pre-expansion. CASE SUMMARY: A 54-year-old male patient presented to the emergency department due to chest pain on June 24, 2019. Within the first 3 minutes of the initial assessment in the emergency room, the electrocardiogram (ECG) showed significant changes. There was atrial fibrillation with ST-segment elevation. Subsequently, atrial fibrillation terminated spontaneously and reverted to sinus rhythm. Soon after, the patient experienced syncope. The ECG revealed torsades de pointes ventricular tachycardia. A few seconds later, it returned to sinus rhythm. High-sensitivity tropon in I was normal. The diagnosis was acute STEMI. Emergency coronary angiography revealed subtotal occlusion with thrombus formation in the proximal segment of the left anterior descending artery. Considering the patient's age and history of peptic ulcer disease, after the intracoronary injection of prourokinase, percutaneous transluminal coronary angioplasty and cutting balloon angioplasty were conducted for thorough preconditioning, and paclitaxel drug-eluting balloon angioplasty was performed without any stents, achieving favorable outcomes. CONCLUSION: A PPCI without stents may be a viable treatment strategy for select patients with STEMI, and further research is warranted.
RESUMO
BACKGROUND: Bradycardia-induced cardiomyopathy (BIC), which is a disease resulting from bradycardia, is characterized by cardiac chamber enlargement and diminished cardiac function. The correction of bradycardia can allow for significant improvements in both cardiac function and structure; however, this disease has been infrequently documented. In this case, we conducted a longitudinal follow-up of a patient who had been enduring BIC for more than 40 years to heighten awareness and prompt timely diagnosis and rational intervention. CASE SUMMARY: A woman who presented with postactivity fatigue and dyspnea was diagnosed with bradycardia at the age of 7. Since she had no obvious symptoms, she did not receive any treatment to improve her bradycardia during the 42-year follow-up, except for the implantation of a temporary pacemaker during labor induction surgery. As time progressed, the patient's heart gradually expanded due to her low ventricular rate, and she was diagnosed with BIC. In 2014, the patient developed atrial fibrillation, her ventricular rate gradually increased, and her heart shape gradually returned to normal. This report describes the cardiac morphological changes caused by the heart rate changes in BIC patients older than 40 years, introduces another possible outcome of BIC, and emphasizes the importance of early intervention in treating BIC. CONCLUSION: BIC can induce atrial fibrillation, causing an increased ventricular rate and leading to positive cardiac remodeling.