{"title":"积液性缩窄性心包炎合并肥厚性心肌病的快速致死性进展和尸检结果。","authors":"Takashi Hiruma, Tatsuya Murai, Masahiro Watanabe, Mamoru Nanasato, Morimasa Takayama, Mitsuaki Isobe","doi":"10.1253/circrep.CR-23-0061","DOIUrl":null,"url":null,"abstract":"patient underwent subxiphoid pericardiocentesis, with 700 mL exudate drained; however, the constrictive echocardiographic findings persisted. The patient remained hemodynamically unstable and eventually died due to multi-organ dysfunction on Day 10 of hospitalization. The autopsy revealed cardiomegaly (heart weight 550 g) and a thickened pericardium (Figure E,F). Myocardial hypertrophy with disarray and interstitial fibrosis was observed, but no other cardiomyopathies were indicated. Notably, both the visceral and parietal pericardium had inflammatory cell infiltration and fibrous thickening (Figure G,H). There was no evidence of infection, autoimmune disease, or maligA 68-year-old man with hypertrophic cardiomyopathy (HCM), chronic atrial fibrillation, and prior pacemaker implantation (at 50 years of age) was referred to the Sakakibara Heart Institute complaining of dyspnea. Computed tomography and transthoracic echocardiography showed significant circumferential pericardial effusion (Figure A,B). The heart presented a swinging motion (Supplementary Movie). The early diastolic mitral flow velocity presented inspiratory decrease and expiratory increase. Furthermore, the early diastolic mitral septal annular velocity (e’) was increased compared with lateral e’, indicating constriction of the heart (Figure C,D). The","PeriodicalId":10276,"journal":{"name":"Circulation Reports","volume":"5 9","pages":"365-366"},"PeriodicalIF":0.0000,"publicationDate":"2023-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/45/48/circrep-5-365.PMC10483110.pdf","citationCount":"0","resultStr":"{\"title\":\"Rapid Fatal Progression and Autopsy Findings of Effusive-Constrictive Pericarditis With Hypertrophic Cardiomyopathy.\",\"authors\":\"Takashi Hiruma, Tatsuya Murai, Masahiro Watanabe, Mamoru Nanasato, Morimasa Takayama, Mitsuaki Isobe\",\"doi\":\"10.1253/circrep.CR-23-0061\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"patient underwent subxiphoid pericardiocentesis, with 700 mL exudate drained; however, the constrictive echocardiographic findings persisted. The patient remained hemodynamically unstable and eventually died due to multi-organ dysfunction on Day 10 of hospitalization. The autopsy revealed cardiomegaly (heart weight 550 g) and a thickened pericardium (Figure E,F). Myocardial hypertrophy with disarray and interstitial fibrosis was observed, but no other cardiomyopathies were indicated. Notably, both the visceral and parietal pericardium had inflammatory cell infiltration and fibrous thickening (Figure G,H). There was no evidence of infection, autoimmune disease, or maligA 68-year-old man with hypertrophic cardiomyopathy (HCM), chronic atrial fibrillation, and prior pacemaker implantation (at 50 years of age) was referred to the Sakakibara Heart Institute complaining of dyspnea. Computed tomography and transthoracic echocardiography showed significant circumferential pericardial effusion (Figure A,B). The heart presented a swinging motion (Supplementary Movie). The early diastolic mitral flow velocity presented inspiratory decrease and expiratory increase. Furthermore, the early diastolic mitral septal annular velocity (e’) was increased compared with lateral e’, indicating constriction of the heart (Figure C,D). The\",\"PeriodicalId\":10276,\"journal\":{\"name\":\"Circulation Reports\",\"volume\":\"5 9\",\"pages\":\"365-366\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2023-09-08\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/45/48/circrep-5-365.PMC10483110.pdf\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Circulation Reports\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.1253/circrep.CR-23-0061\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Circulation Reports","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1253/circrep.CR-23-0061","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Rapid Fatal Progression and Autopsy Findings of Effusive-Constrictive Pericarditis With Hypertrophic Cardiomyopathy.
patient underwent subxiphoid pericardiocentesis, with 700 mL exudate drained; however, the constrictive echocardiographic findings persisted. The patient remained hemodynamically unstable and eventually died due to multi-organ dysfunction on Day 10 of hospitalization. The autopsy revealed cardiomegaly (heart weight 550 g) and a thickened pericardium (Figure E,F). Myocardial hypertrophy with disarray and interstitial fibrosis was observed, but no other cardiomyopathies were indicated. Notably, both the visceral and parietal pericardium had inflammatory cell infiltration and fibrous thickening (Figure G,H). There was no evidence of infection, autoimmune disease, or maligA 68-year-old man with hypertrophic cardiomyopathy (HCM), chronic atrial fibrillation, and prior pacemaker implantation (at 50 years of age) was referred to the Sakakibara Heart Institute complaining of dyspnea. Computed tomography and transthoracic echocardiography showed significant circumferential pericardial effusion (Figure A,B). The heart presented a swinging motion (Supplementary Movie). The early diastolic mitral flow velocity presented inspiratory decrease and expiratory increase. Furthermore, the early diastolic mitral septal annular velocity (e’) was increased compared with lateral e’, indicating constriction of the heart (Figure C,D). The