Fabry disease is an important secondary cardiomyopathy characterized by the accumulation of glycosphingolipids due to a pathogenic mutation in the GLA gene. Lethal ventricular arrhythmia is the most common cause of sudden death in patients with Fabry disease. We herein report a case of a man in his 40s with late-onset Fabry disease who had polymorphic ventricular tachycardia and fibrillation during enzyme replacement therapy. After recovery from successful cardiopulmonary resuscitation, we recommended implantation of an implantable cardioverter-defibrillator; however, the patient refused to undergo implantation at that time. We administered a wearable cardioverter-defibrillator at his discharge, and he was successfully rescued from polymorphic ventricular tachycardia and fibrillation. He was finally given an implantable cardioverter-defibrillator.
Learning objective
In Fabry disease, lethal ventricular arrhythmia is an important cause of sudden death. Ventricular tachycardia and fibrillation during enzyme replacement therapy have not been reported. Furthermore, secondary prevention of lethal ventricular arrhythmia using a wearable cardioverter-defibrillator has not been reported in Fabry disease. Therefore, this case report has implications for the possible incidence and prevention of lethal ventricular arrhythmias in patients with Fabry disease.
{"title":"Rescue from sudden ventricular tachycardia and fibrillation using wearable cardioverter-defibrillator in male late-onset Fabry disease patient","authors":"Toraaki Okuyama MD , Eiko Fukuro MD , Kenichi Tokutake MD, PhD , Masahisa Kobayashi MD, PhD , Hiroshi Kobayashi MD, PhD , Michihiro Yoshimura MD, PhD, FJCC , Kenichi Hongo MD, PhD","doi":"10.1016/j.jccase.2024.11.004","DOIUrl":"10.1016/j.jccase.2024.11.004","url":null,"abstract":"<div><div>Fabry disease is an important secondary cardiomyopathy characterized by the accumulation of glycosphingolipids due to a pathogenic mutation in the <em>GLA</em> gene. Lethal ventricular arrhythmia is the most common cause of sudden death in patients with Fabry disease. We herein report a case of a man in his 40s with late-onset Fabry disease who had polymorphic ventricular tachycardia and fibrillation during enzyme replacement therapy. After recovery from successful cardiopulmonary resuscitation, we recommended implantation of an implantable cardioverter-defibrillator; however, the patient refused to undergo implantation at that time. We administered a wearable cardioverter-defibrillator at his discharge, and he was successfully rescued from polymorphic ventricular tachycardia and fibrillation. He was finally given an implantable cardioverter-defibrillator.</div></div><div><h3>Learning objective</h3><div>In Fabry disease, lethal ventricular arrhythmia is an important cause of sudden death. Ventricular tachycardia and fibrillation during enzyme replacement therapy have not been reported. Furthermore, secondary prevention of lethal ventricular arrhythmia using a wearable cardioverter-defibrillator has not been reported in Fabry disease. Therefore, this case report has implications for the possible incidence and prevention of lethal ventricular arrhythmias in patients with Fabry disease.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 53-56"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pemafibrate is a selective peroxisome proliferator-activated receptor alpha (PPARα) activator. Pemafibrate has been shown to reduce serum triglyceride levels to an equivalent or greater extent than traditional fibrates, with a lower incidence of drug-related adverse events. Pemafibrate may have the potential to improve clinical outcomes in carefully selected patients with cardiovascular diseases by ameliorating dyslipidemia and stabilizing systemic arteriosclerosis. Additionally, several experimental studies have demonstrated a novel potential for pemafibrate in improving heart failure through its pleiotropic effects. We encountered two patients with systolic heart failure that was refractory to guideline-directed medical therapy. Both patients experienced further cardiac reverse remodeling and an improvement in hypertriglyceridemia following a six-month course of pemafibrate add-on therapy. Pemafibrate might facilitate cardiac reverse remodeling when incorporated into conventional heart failure medications. Further prospective randomized controlled studies are warranted to evaluate the clinical implications of incorporating pemafibrate into medical therapy for heart failure patients. Future research should also explore the long-term effects of pemafibrate on cardiovascular outcomes, the underlying mechanisms of its pleiotropic benefits, and its efficacy in diverse patient populations to solidify its role in heart failure management.
Learning objective
Pemafibrate, a recently introduced selective peroxisome proliferator-activated receptor alpha activator that improves hypertriglyceridemia, may facilitate cardiac reverse remodeling when incorporated into conventional heart failure medications.
{"title":"Pemafibrate and cardiac reverse remodeling in patients with systolic heart failure receiving guideline-directed medical therapy","authors":"Yuki Hida MD, Teruhiko Imamura MD, PhD, FJCC, Koichiro Kinugawa MD, PhD, FJCC","doi":"10.1016/j.jccase.2024.10.001","DOIUrl":"10.1016/j.jccase.2024.10.001","url":null,"abstract":"<div><div>Pemafibrate is a selective peroxisome proliferator-activated receptor alpha (PPARα) activator. Pemafibrate has been shown to reduce serum triglyceride levels to an equivalent or greater extent than traditional fibrates, with a lower incidence of drug-related adverse events. Pemafibrate may have the potential to improve clinical outcomes in carefully selected patients with cardiovascular diseases by ameliorating dyslipidemia and stabilizing systemic arteriosclerosis. Additionally, several experimental studies have demonstrated a novel potential for pemafibrate in improving heart failure through its pleiotropic effects. We encountered two patients with systolic heart failure that was refractory to guideline-directed medical therapy. Both patients experienced further cardiac reverse remodeling and an improvement in hypertriglyceridemia following a six-month course of pemafibrate add-on therapy. Pemafibrate might facilitate cardiac reverse remodeling when incorporated into conventional heart failure medications. Further prospective randomized controlled studies are warranted to evaluate the clinical implications of incorporating pemafibrate into medical therapy for heart failure patients. Future research should also explore the long-term effects of pemafibrate on cardiovascular outcomes, the underlying mechanisms of its pleiotropic benefits, and its efficacy in diverse patient populations to solidify its role in heart failure management.</div></div><div><h3>Learning objective</h3><div>Pemafibrate, a recently introduced selective peroxisome proliferator-activated receptor alpha activator that improves hypertriglyceridemia, may facilitate cardiac reverse remodeling when incorporated into conventional heart failure medications.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 42-45"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149308","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Inferior vena cava (IVC) filters are sometimes implanted in patients with deep vein thrombosis (DVT) to prevent pulmonary embolism (PE). Long-term filter placement is associated with various complications and retrieval failure using conventional methods. We describe a novel method for retrieval of long-term implanted IVC filters. A 41-year-old woman was diagnosed with left common iliac DVT. A temporary IVC filter was implanted to prevent life-threatening PE in parallel with anticoagulation therapy, followed by the long-term retrievable IVC filter (Denali, Bard Medical, Georgia, IN, USA). After successful anticoagulation therapy, the retrieval of the Denali by conventional methods failed due to adhesion to the vessel wall. We decided to remove the Denali using pacemaker lead extraction methods. Twenty months after the Denali implantation, extraction was performed under general anesthesia. A snare catheter (Lassos, Osypka, Berlin, Germany) was used to capture the proximal hook. The severe adhesions around the anchors were carefully dissected using a mechanical sheath (Byrd Dilator Sheaths, Cook Medical, Bloomington, IN, USA). The Denali was extracted using the counter-traction technique. The post-operative course was uneventful. This technique may be useful for uneventful removal of long-term implanted IVC filters, potentially avoiding open surgery. Additional experience is needed to overcome the limitation of a single case report.
Learning objective
Inferior vena cava (IVC) filters are sometimes used to reduce the risk of life-threatening pulmonary embolism. Long-term implanted IVC filters are associated with filter-related complications and can be difficult to remove by conventional methods due to adhesion around the filter. We describe a novel IVC filter retrieval technique using pacemaker lead extraction tools that has the potential to avoid highly invasive open surgery.
{"title":"Advanced retrieval technique using pacemaker lead extraction methods for a long-term implanted inferior vena cava filter with caval penetration of the pancreas","authors":"Yasuhiro Shimotori MD , Ayako Okada MD, PhD , Koji Yoshie MD, PhD , Takanori Tomatsu MD , Sho Suzuki MD , Kiu Tanaka MD , Toshinori Komatsu MD , Keisuke Machida MD , Hideki Kobayashi MD, PhD , Yasutaka Oguchi MD, PhD , Tatsuya Saigusa MD, PhD , Souichiro Ebisawa MD, PhD , Hirohiko Motoki MD, PhD , Morio Shoda MD, PhD , Koichiro Kuwahara MD, PhD, FJCC","doi":"10.1016/j.jccase.2024.11.001","DOIUrl":"10.1016/j.jccase.2024.11.001","url":null,"abstract":"<div><div>Inferior vena cava (IVC) filters are sometimes implanted in patients with deep vein thrombosis (DVT) to prevent pulmonary embolism (PE). Long-term filter placement is associated with various complications and retrieval failure using conventional methods. We describe a novel method for retrieval of long-term implanted IVC filters. A 41-year-old woman was diagnosed with left common iliac DVT. A temporary IVC filter was implanted to prevent life-threatening PE in parallel with anticoagulation therapy, followed by the long-term retrievable IVC filter (Denali, Bard Medical, Georgia, IN, USA). After successful anticoagulation therapy, the retrieval of the Denali by conventional methods failed due to adhesion to the vessel wall. We decided to remove the Denali using pacemaker lead extraction methods. Twenty months after the Denali implantation, extraction was performed under general anesthesia. A snare catheter (Lassos, Osypka, Berlin, Germany) was used to capture the proximal hook. The severe adhesions around the anchors were carefully dissected using a mechanical sheath (Byrd Dilator Sheaths, Cook Medical, Bloomington, IN, USA). The Denali was extracted using the counter-traction technique. The post-operative course was uneventful. This technique may be useful for uneventful removal of long-term implanted IVC filters, potentially avoiding open surgery. Additional experience is needed to overcome the limitation of a single case report.</div></div><div><h3>Learning objective</h3><div>Inferior vena cava (IVC) filters are sometimes used to reduce the risk of life-threatening pulmonary embolism. Long-term implanted IVC filters are associated with filter-related complications and can be difficult to remove by conventional methods due to adhesion around the filter. We describe a novel IVC filter retrieval technique using pacemaker lead extraction tools that has the potential to avoid highly invasive open surgery.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 49-52"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Left main compression syndrome (LMCS) is a disease in which the ostium of the left main coronary artery is compressed between a dilated pulmonary artery and the sinus of Valsalva associated with pulmonary hypertension (PH). The major etiology of LMCS is secondary PH due to congenital heart disease. However, no reports exist regarding LMCS caused by PH due to peripheral pulmonary artery stenosis complicated with moyamoya disease (MMD). We report a case of LMCS caused by PH due to peripheral pulmonary artery stenosis complicated with MMD in a 41-year-old woman who was treated with percutaneous coronary intervention.
Learning objective
Left main compression syndrome (LMCS) is a condition in which the main trunk of the left coronary artery is compressed between the dilated pulmonary artery and aorta due to pulmonary hypertension. This paper reports the first case of LMCS due to peripheral pulmonary artery stenosis complicated with moyamoya disease.
{"title":"Left main compression syndrome caused by pulmonary hypertension due to peripheral pulmonary artery stenosis complicated with moyamoya disease","authors":"Sei Matsuo MD, Kazuyuki Ozaki MD, FJCC, Takeshi Kashimura MD, Yuji Matsuo MD, Tsugumi Takayama MD, Makoto Hoyano MD, Takao Yanagawa MD, Takayuki Inomata MD, FJCC","doi":"10.1016/j.jccase.2024.09.006","DOIUrl":"10.1016/j.jccase.2024.09.006","url":null,"abstract":"<div><div>Left main compression syndrome (LMCS) is a disease in which the ostium of the left main coronary artery is compressed between a dilated pulmonary artery and the sinus of Valsalva associated with pulmonary hypertension (PH). The major etiology of LMCS is secondary PH due to congenital heart disease. However, no reports exist regarding LMCS caused by PH due to peripheral pulmonary artery stenosis complicated with moyamoya disease (MMD). We report a case of LMCS caused by PH due to peripheral pulmonary artery stenosis complicated with MMD in a 41-year-old woman who was treated with percutaneous coronary intervention.</div></div><div><h3>Learning objective</h3><div>Left main compression syndrome (LMCS) is a condition in which the main trunk of the left coronary artery is compressed between the dilated pulmonary artery and aorta due to pulmonary hypertension. This paper reports the first case of LMCS due to peripheral pulmonary artery stenosis complicated with moyamoya disease.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 29-34"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143150251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A 47-year-old woman with exertional dyspnea was admitted to our hospital. Echocardiography revealed congestive heart failure (HF), with reduced left ventricular ejection fraction (13 %) and elevated brain natriuretic peptide levels (877 pg/mL). The patient underwent medical therapy and comprehensive cardiac rehabilitation (CR). At discharge, the oxygen uptake at anaerobic threshold (AT) was 13.1 mL/kg/min. Outpatient CR consisted of exercise therapy, patient education, and home activity intensity instructions with pulse rate (PR) management using a wearable device. We instructed that activity intensity at home should not exceed the PR at AT. Two months after discharge, the patient's condition was stable, and she was compliant with activity intensity restrictions; therefore, she was allowed to return to work twice a week for 5 h of light work weekly, which was gradually increased. We continued to monitor the PR with wearable devices to ensure compliance with work intensity. Five months after discharge, she achieved a return to work four times a week for 8 h without exacerbation of HF symptoms. The workplace was receptive to the suggestions of the CR team regarding workplace conditions, safe working hours, and frequency, and the patient successfully returned to work, achieving a balance between treatment and work.
Learning objective
The use of comprehensive cardiac rehabilitation is recommended for the return to work by patients with heart failure. However, specific measures to manage activity intensity for return to work have not been considered fully. The strategy that we adopted involved a combination of comprehensive cardiac rehabilitation and the use of wearable devices for guided work intensity management, allowing for a balance between treatment and work responsibilities.
{"title":"Comprehensive cardiac rehabilitation utilized to support patients with heart failure for balancing treatment and work: A case report","authors":"Kazufumi Kitagaki (PhD) , Yuji Hongo (MSc) , Rie Futai (PhD) , Takeshi Hasegawa (RPT) , Tatsuyoshi Azuma (BSc) , Hiroshi Morikawa (BSc) , Hazuki Koizumi (Ns) , Takuya Kiyohara (MD) , Hisashi Shimoyama (PhD)","doi":"10.1016/j.jccase.2024.10.003","DOIUrl":"10.1016/j.jccase.2024.10.003","url":null,"abstract":"<div><div>A 47-year-old woman with exertional dyspnea was admitted to our hospital. Echocardiography revealed congestive heart failure (HF), with reduced left ventricular ejection fraction (13 %) and elevated brain natriuretic peptide levels (877 pg/mL). The patient underwent medical therapy and comprehensive cardiac rehabilitation (CR). At discharge, the oxygen uptake at anaerobic threshold (AT) was 13.1 mL/kg/min. Outpatient CR consisted of exercise therapy, patient education, and home activity intensity instructions with pulse rate (PR) management using a wearable device. We instructed that activity intensity at home should not exceed the PR at AT. Two months after discharge, the patient's condition was stable, and she was compliant with activity intensity restrictions; therefore, she was allowed to return to work twice a week for 5 h of light work weekly, which was gradually increased. We continued to monitor the PR with wearable devices to ensure compliance with work intensity. Five months after discharge, she achieved a return to work four times a week for 8 h without exacerbation of HF symptoms. The workplace was receptive to the suggestions of the CR team regarding workplace conditions, safe working hours, and frequency, and the patient successfully returned to work, achieving a balance between treatment and work.</div></div><div><h3>Learning objective</h3><div>The use of comprehensive cardiac rehabilitation is recommended for the return to work by patients with heart failure. However, specific measures to manage activity intensity for return to work have not been considered fully. The strategy that we adopted involved a combination of comprehensive cardiac rehabilitation and the use of wearable devices for guided work intensity management, allowing for a balance between treatment and work responsibilities.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 35-38"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143150252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We present a case of squamous cell carcinoma of unknown primary (SCCUP) with metastasis to the right ventricle (RV) successfully treated through surgical resection and postoperative chemotherapy with an immune checkpoint inhibitor (ICI). A 50-year-old woman presented with dyspnea, prompting transthoracic echocardiography that revealed a mobile, irregular RV mass measuring 40 × 32 mm. Contrast-enhanced computed tomography (CT) revealed masses in the RV and the right pulmonary artery, which was totally occluded. Emergency surgical resection of both masses was performed to avoid sudden death. Histopathological analysis confirmed squamous cell carcinoma; however, the primary origin of the masses remained unidentified despite extensive evaluations, including positron emission tomography-CT. The final diagnosis was SCCUP. Immunohistochemistry indicated positive programmed cell death ligand 1, and postoperative chemotherapy with an ICI was administered. One year post-surgery, the patient remains healthy with no sign of recurrence.
Learning objective
This case shows the treatment of squamous cell carcinoma of unknown primary (SCCUP) with cardiac metastasis through emergency surgery and postoperative immunotherapy. Despite the poor prognosis associated with cardiac metastatic malignant tumors and the lack of established treatment guidelines, this case highlights the potential benefits of surgical intervention and the efficacy of immunotherapy in managing cardiac metastatic SCCUP, with the patient remaining with no recurrence one-year post-surgery.
{"title":"Effectiveness of surgery and chemotherapy with immune checkpoint inhibitor for cardiac metastatic squamous cell carcinoma of unknown primary","authors":"Akito Kuwano MD , Masaru Yoshikai MD, PhD , Satoshi Ohtsubo MD, PhD , Kiyokazu Koga MD, PhD , Nozomi Yoshida MD , Naoyo Nishida MD, PhD","doi":"10.1016/j.jccase.2024.10.002","DOIUrl":"10.1016/j.jccase.2024.10.002","url":null,"abstract":"<div><div>We present a case of squamous cell carcinoma of unknown primary (SCCUP) with metastasis to the right ventricle (RV) successfully treated through surgical resection and postoperative chemotherapy with an immune checkpoint inhibitor (ICI). A 50-year-old woman presented with dyspnea, prompting transthoracic echocardiography that revealed a mobile, irregular RV mass measuring 40 × 32 mm. Contrast-enhanced computed tomography (CT) revealed masses in the RV and the right pulmonary artery, which was totally occluded. Emergency surgical resection of both masses was performed to avoid sudden death. Histopathological analysis confirmed squamous cell carcinoma; however, the primary origin of the masses remained unidentified despite extensive evaluations, including positron emission tomography-CT. The final diagnosis was SCCUP. Immunohistochemistry indicated positive programmed cell death ligand 1, and postoperative chemotherapy with an ICI was administered. One year post-surgery, the patient remains healthy with no sign of recurrence.</div></div><div><h3>Learning objective</h3><div>This case shows the treatment of squamous cell carcinoma of unknown primary (SCCUP) with cardiac metastasis through emergency surgery and postoperative immunotherapy. Despite the poor prognosis associated with cardiac metastatic malignant tumors and the lack of established treatment guidelines, this case highlights the potential benefits of surgical intervention and the efficacy of immunotherapy in managing cardiac metastatic SCCUP, with the patient remaining with no recurrence one-year post-surgery.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 39-41"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149310","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A 72-year-old woman undergoing hemodialysis presented with effort angina pectoris due to severe stenosis with calcified nodules in the right coronary artery. Percutaneous coronary intervention was performed using an excimer laser coronary angioplasty and an ultrathin-strut covered stent (CS) was implanted due to coronary perforation. An additional durable-polymer everolimus-eluting stent (DP-EES) was implanted because of protrusions in the proximal edge of the CS. However, late stent thrombosis occurred six months after ultrathin-strut covered stent implantation for a calcified nodule. After thrombus aspiration, intravascular imaging analyses revealed that the struts within the CS were fully covered with thick neointimal hyperplasia. In contrast, half of the struts in the DP-EES were uncovered and some struts were malapposed. In this case, we speculated that the cause of the current late stent thrombosis was dispersion of the thrombi formed at the uncovered with malapposed sites in the DP-EES into a severe stenosis caused by neointimal hyperplasia in the CS. Neointimal hyperplasia occurs at the edge of the CS, a CS should be implanted locating its edge on the site with less plaque.
Learning objectives
•
To evaluate the mechanism of late stent thrombosis after ultrathin strut-covered stent implantation for lesions with calcified nodules.
•
To discuss the optimal covered stent placement locating its edge on the site with less plaque.
•
To recognize that introduction of an ultrathin-strut covered stent for lesions with calcified nodules requires careful consideration.
{"title":"Late stent thrombosis six months after ultrathin-strut covered stent implantation in lesion with calcified nodule","authors":"Naoko Higashino MD, Takayuki Ishihara MD, Takuya Tsujimura MD, Yosuke Hata MD, Sho Nakao MD, Masaya Kusuda MD, Toshiaki Mano MD, PhD","doi":"10.1016/j.jccase.2024.11.002","DOIUrl":"10.1016/j.jccase.2024.11.002","url":null,"abstract":"<div><div>A 72-year-old woman undergoing hemodialysis presented with effort angina pectoris due to severe stenosis with calcified nodules in the right coronary artery. Percutaneous coronary intervention was performed using an excimer laser coronary angioplasty and an ultrathin-strut covered stent (CS) was implanted due to coronary perforation. An additional durable-polymer everolimus-eluting stent (DP-EES) was implanted because of protrusions in the proximal edge of the CS. However, late stent thrombosis occurred six months after ultrathin-strut covered stent implantation for a calcified nodule. After thrombus aspiration, intravascular imaging analyses revealed that the struts within the CS were fully covered with thick neointimal hyperplasia. In contrast, half of the struts in the DP-EES were uncovered and some struts were malapposed. In this case, we speculated that the cause of the current late stent thrombosis was dispersion of the thrombi formed at the uncovered with malapposed sites in the DP-EES into a severe stenosis caused by neointimal hyperplasia in the CS. Neointimal hyperplasia occurs at the edge of the CS, a CS should be implanted locating its edge on the site with less plaque.</div></div><div><h3>Learning objectives</h3><div><ul><li><span>•</span><span><div>To evaluate the mechanism of late stent thrombosis after ultrathin strut-covered stent implantation for lesions with calcified nodules.</div></span></li><li><span>•</span><span><div>To discuss the optimal covered stent placement locating its edge on the site with less plaque.</div></span></li><li><span>•</span><span><div>To recognize that introduction of an ultrathin-strut covered stent for lesions with calcified nodules requires careful consideration.</div></span></li></ul></div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 2","pages":"Pages 46-48"},"PeriodicalIF":0.0,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143149311","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Myocarditis and pericarditis, or myopericarditis, is a rare, albeit life-threatening, cardiac complication of coronavirus disease 2019 (COVID-19). Although most patients recover from myocardial inflammation within weeks of the acute infection, there are concerns about acute and long-term myocardial injury. Coronary microvascular dysfunction and myocardial inflammation in the affected myocardium might be key factors in developing acute COVID-19-associated myopericarditis. In this case report, we describe a 38-year-old woman diagnosed with acute COVID-19-associated myopericarditis who was treated successfully. This case highlights the remarkable recovery in coronary microcirculation and myocardial inflammation assessed using multi-imaging modalities from the acute phase to 3-month follow-up using histopathological assessments.
Learning objective
Acute myopericarditis is one of the serious cardiac complications associated with severe acute respiratory syndrome coronavirus 2 infection, although an accurate diagnosis might be challenging. We emphasize a novel combination of magnetic resonance imaging and positron emission tomography focusing on serial changes in coronary microcirculation and myocardial inflammation from acute to recovery phases. Our findings may elucidate the pathophysiology of this entity at the micro and macro levels.
{"title":"Impaired myocardial perfusion and myocardial inflammation of acute myopericarditis associated with COVID-19","authors":"Shiro Miura MD, PhD , Kisaki Amemiya MD, PhD , Atsutaka Okizaki MD, PhD , Osamu Manabe MD, PhD , Shingo Tsujinaga MD, PhD , Chihoko Miyazaki MD, PhD , Yoshihiko Ikeda MD, PhD , Kinta Hatakeyama MD, PhD , Shuji Takahashi MD, PhD , Takehiro Yamashita MD, PhD","doi":"10.1016/j.jccase.2024.09.008","DOIUrl":"10.1016/j.jccase.2024.09.008","url":null,"abstract":"<div><div>Myocarditis and pericarditis, or myopericarditis, is a rare, albeit life-threatening, cardiac complication of coronavirus disease 2019 (COVID-19). Although most patients recover from myocardial inflammation within weeks of the acute infection, there are concerns about acute and long-term myocardial injury. Coronary microvascular dysfunction and myocardial inflammation in the affected myocardium might be key factors in developing acute COVID-19-associated myopericarditis. In this case report, we describe a 38-year-old woman diagnosed with acute COVID-19-associated myopericarditis who was treated successfully. This case highlights the remarkable recovery in coronary microcirculation and myocardial inflammation assessed using multi-imaging modalities from the acute phase to 3-month follow-up using histopathological assessments.</div></div><div><h3>Learning objective</h3><div>Acute myopericarditis is one of the serious cardiac complications associated with severe acute respiratory syndrome coronavirus 2 infection, although an accurate diagnosis might be challenging. We emphasize a novel combination of magnetic resonance imaging and positron emission tomography focusing on serial changes in coronary microcirculation and myocardial inflammation from acute to recovery phases. Our findings may elucidate the pathophysiology of this entity at the micro and macro levels.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 1","pages":"Pages 12-16"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143015534","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
The incidence of invasive group A Streptococcus (iGAS) infection has been increasing across all age groups, including pediatric patients, and is associated with high mortality rates. Although iGAS infection leads to streptococcal toxic shock syndrome and necrotizing soft tissue infections, iGAS-associated infective endocarditis (IE) is rare. Here, we report a case of iGAS-associated IE, streptococcal toxic shock syndrome, and pyomyositis that occurred after the Fontan procedure in a 7-year-old patient. Initial treatment included antibiotics and surgical intervention for pyomyositis. Despite her overall condition's improvement, persistent fever led to the discovery of IE. Furthermore, this patient developed cardiac rupture due to the progression of IE but was successfully rescued. No neurological complications occurred, and the patient was discharged without recurrence of infection. To our knowledge, this is the first case report of successful life-saving treatment for cardiac rupture due to IE caused by iGAS in a pediatric Fontan patient. This case suggests that iGAS infections in patients with complex congenital heart disease warrant a crucial search for complications of iGAS-associated IE.
Learning objective
The incidence of invasive group A Streptococcus (iGAS) infection is increasing globally. While infective endocarditis (IE) caused by iGAS is rare, the risk may be elevated among patients with complex congenital heart disease. This underscores the importance of searching for iGAS-associated IE and the need for treatment with consideration for exacerbation.
{"title":"Cardiac rupture and toxic shock syndrome by invasive group a Streptococcus in a Fontan patient with Asplenia syndrome","authors":"Mamoru Muraoka MD , Kenichi Tetsuhara MD, PhD , Sayo Suzuki MD , Kenichiro Yamamura MD, PhD , Toshihide Nakano MD, PhD , Sagano Onoyama MD, PhD , Koichi Sagawa MD, PhD","doi":"10.1016/j.jccase.2024.09.009","DOIUrl":"10.1016/j.jccase.2024.09.009","url":null,"abstract":"<div><div>The incidence of invasive group A Streptococcus (iGAS) infection has been increasing across all age groups, including pediatric patients, and is associated with high mortality rates. Although iGAS infection leads to streptococcal toxic shock syndrome and necrotizing soft tissue infections, iGAS-associated infective endocarditis (IE) is rare. Here, we report a case of iGAS-associated IE, streptococcal toxic shock syndrome, and pyomyositis that occurred after the Fontan procedure in a 7-year-old patient. Initial treatment included antibiotics and surgical intervention for pyomyositis. Despite her overall condition's improvement, persistent fever led to the discovery of IE. Furthermore, this patient developed cardiac rupture due to the progression of IE but was successfully rescued. No neurological complications occurred, and the patient was discharged without recurrence of infection. To our knowledge, this is the first case report of successful life-saving treatment for cardiac rupture due to IE caused by iGAS in a pediatric Fontan patient. This case suggests that iGAS infections in patients with complex congenital heart disease warrant a crucial search for complications of iGAS-associated IE.</div></div><div><h3>Learning objective</h3><div>The incidence of invasive group A Streptococcus (iGAS) infection is increasing globally. While infective endocarditis (IE) caused by iGAS is rare, the risk may be elevated among patients with complex congenital heart disease. This underscores the importance of searching for iGAS-associated IE and the need for treatment with consideration for exacerbation.</div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 1","pages":"Pages 24-28"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143016151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
There are some reports of atrial screw-in lead perforation, but the entire lead body is rarely exposed outside the right atrium at an early stage of the procedure. A man in his 80s had undergone catheter ablation for atrial fibrillation (AF) and had recurrent AF and tachycardia-bradycardia syndrome with 8.8 s of sinus arrest, which caused presyncope. The day after the dual-chamber pacemaker was implanted, atrial screw-in lead perforation caused an elevated threshold, a right pneumothorax, bloody pleural effusion, and pneumomediastinum. A small right thoracotomy with thoracoscopy was performed. The lead that completely penetrated the right atrial appendage and was exposed was safely retracted into the heart and removed thoracoscopically. Early surgery is essential when complete lead perforation with elevated threshold is suspected.
Learning objectives
1.
Perforation of the right atrium by the screw-in lead causes contralateral pneumothorax and chest hemorrhage.
2.
Elevated lead threshold suggests lead perforation outside the myocardium.
3.
Treatment was possible with a small right thoracotomy combined with thoracoscopy.
{"title":"Complete atrial screw lead penetration and contralateral pneumothorax post-pacemaker implantation","authors":"Satoko Shiomi MD, Michifumi Tokuda MD, PhD, Hidenori Sato MD, PhD, Kenichi Tokutake MD, PhD, Seigo Yamashita MD, PhD, Michihiro Yoshimura MD, PhD, FJCC, Teiichi Yamane MD, PhD","doi":"10.1016/j.jccase.2024.09.002","DOIUrl":"10.1016/j.jccase.2024.09.002","url":null,"abstract":"<div><div>There are some reports of atrial screw-in lead perforation, but the entire lead body is rarely exposed outside the right atrium at an early stage of the procedure. A man in his 80s had undergone catheter ablation for atrial fibrillation (AF) and had recurrent AF and tachycardia-bradycardia syndrome with 8.8 s of sinus arrest, which caused presyncope. The day after the dual-chamber pacemaker was implanted, atrial screw-in lead perforation caused an elevated threshold, a right pneumothorax, bloody pleural effusion, and pneumomediastinum. A small right thoracotomy with thoracoscopy was performed. The lead that completely penetrated the right atrial appendage and was exposed was safely retracted into the heart and removed thoracoscopically. Early surgery is essential when complete lead perforation with elevated threshold is suspected.</div></div><div><h3>Learning objectives</h3><div><ul><li><span>1.</span><span><div>Perforation of the right atrium by the screw-in lead causes contralateral pneumothorax and chest hemorrhage.</div></span></li><li><span>2.</span><span><div>Elevated lead threshold suggests lead perforation outside the myocardium.</div></span></li><li><span>3.</span><span><div>Treatment was possible with a small right thoracotomy combined with thoracoscopy.</div></span></li></ul></div></div>","PeriodicalId":52092,"journal":{"name":"Journal of Cardiology Cases","volume":"31 1","pages":"Pages 1-4"},"PeriodicalIF":0.0,"publicationDate":"2025-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143069603","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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