Pub Date : 2020-11-06DOI: 10.3390/cardiogenetics10020007
Z. Ahmadihosseini, Morteza Moeinian, S. Nazemi, S. Elyasi, A. Mohammadpour
Objectives: Fetuin-A is a circulating calcification inhibitor that prevents coronary artery calcification (CAC) by increasing calcium phosphate solubility and inhibiting VSMC differentiation and apoptosis. In this study, we investigated the correlation between rs4918 and CAC in patients with coronary artery disease (CAD). Methods: Forty-two healthy individuals and eighty-one CAD patients were recruited in the present study. The CAC score (CACS) was measured by CT angiography and the genotype analysis of rs4918 single-nucleotide polymorphism SNP was performed by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: The CACS was significantly higher in CAD patients compared to healthy individuals (p < 0.001); however, there was no significant difference between the mean CACS in the presence and absence of rs4918 (p = 0.792). The mean calcium score of the left main coronary artery (LMCA) was significantly lower in carriers of the rs4918 allele (p = 0.036). The frequency of rs4918 SNP was almost similar in the control group and CAD patients (p = 0.846). Conclusions: in patients with CAD, we found no significant association between rs4918 SNP and CACS, indicating that carriers of this allele are not at increased risk of developing cardiovascular diseases compared with those without.
{"title":"Evaluation of the Correlation between the rs4918 Polymorphism of AHSG Gene and Coronary Artery Calcification in Patients with Coronary Artery Disease","authors":"Z. Ahmadihosseini, Morteza Moeinian, S. Nazemi, S. Elyasi, A. Mohammadpour","doi":"10.3390/cardiogenetics10020007","DOIUrl":"https://doi.org/10.3390/cardiogenetics10020007","url":null,"abstract":"Objectives: Fetuin-A is a circulating calcification inhibitor that prevents coronary artery calcification (CAC) by increasing calcium phosphate solubility and inhibiting VSMC differentiation and apoptosis. In this study, we investigated the correlation between rs4918 and CAC in patients with coronary artery disease (CAD). Methods: Forty-two healthy individuals and eighty-one CAD patients were recruited in the present study. The CAC score (CACS) was measured by CT angiography and the genotype analysis of rs4918 single-nucleotide polymorphism SNP was performed by the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: The CACS was significantly higher in CAD patients compared to healthy individuals (p < 0.001); however, there was no significant difference between the mean CACS in the presence and absence of rs4918 (p = 0.792). The mean calcium score of the left main coronary artery (LMCA) was significantly lower in carriers of the rs4918 allele (p = 0.036). The frequency of rs4918 SNP was almost similar in the control group and CAD patients (p = 0.846). Conclusions: in patients with CAD, we found no significant association between rs4918 SNP and CACS, indicating that carriers of this allele are not at increased risk of developing cardiovascular diseases compared with those without.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2020-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/cardiogenetics10020007","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48635571","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}
Pub Date : 2020-11-04DOI: 10.3390/cardiogenetics10020006
M. Singh, A. Gomes, Moad El-Haddad, A. Saidmeerasah, R. Iqbal
Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is a rare coronary artery anomaly which accounts for 0.25–0.5% of all congenital cardiac diseases, where most die within the first year of life. We present a case report of a 50-year-old lady who presented to hospital with persistent palpitations. Her admission electrocardiogram found her to be in Atrial Fibrillation (AF). She was rate-controlled and subsequently discharged. Despite that, she represented with further episodes of AF and was referred for an outpatient transthoracic echocardiogram. This revealed a dilated right coronary artery, retrograde flow in the left coronary artery and collateral flow in the myocardium. To investigate, the patient had undergone further imaging which confirmed the diagnosis. As such, she was later shortlisted for surgical intervention. Conclusively, our case exemplifies the role of multimodal imaging to identify the features of ALCAPA and may be useful for the purposes of surgical intervention.
{"title":"Anomalous Left Coronary Artery from the Pulmonary Artery: The Role of Multimodal Imaging—A Case Report","authors":"M. Singh, A. Gomes, Moad El-Haddad, A. Saidmeerasah, R. Iqbal","doi":"10.3390/cardiogenetics10020006","DOIUrl":"https://doi.org/10.3390/cardiogenetics10020006","url":null,"abstract":"Anomalous Left Coronary Artery from the Pulmonary Artery (ALCAPA) is a rare coronary artery anomaly which accounts for 0.25–0.5% of all congenital cardiac diseases, where most die within the first year of life. We present a case report of a 50-year-old lady who presented to hospital with persistent palpitations. Her admission electrocardiogram found her to be in Atrial Fibrillation (AF). She was rate-controlled and subsequently discharged. Despite that, she represented with further episodes of AF and was referred for an outpatient transthoracic echocardiogram. This revealed a dilated right coronary artery, retrograde flow in the left coronary artery and collateral flow in the myocardium. To investigate, the patient had undergone further imaging which confirmed the diagnosis. As such, she was later shortlisted for surgical intervention. Conclusively, our case exemplifies the role of multimodal imaging to identify the features of ALCAPA and may be useful for the purposes of surgical intervention.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":"1 1","pages":""},"PeriodicalIF":0.6,"publicationDate":"2020-11-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3390/cardiogenetics10020006","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41843436","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}
Pub Date : 2020-04-07DOI: 10.4081/cardiogenetics.2020.8860
C. Mazzaccara, Bruno Mirra, Ferdinando Barretta, B. Lombardo, O. Scudiero, G. Frisso
Intense athletic training and competition can rarely result in sudden cardiac death (SCD). Despite the introduction of pre-participation cardiovascular screening, especially among young competitive athletes, sport-related SCD remains a debated issue among medical personnel, sports communities and laypersons alike, and generates significant media attention. The most frequent cause of SCD is a hidden inherited cardiomyopathy, the athletes may not even be aware of. Predictive medicine, by searching the presence of pathogenic alterations in cardiac genes, may be an integrative tool, besides the conventional ones used in cardiology (mainly electro and echocardiogram), to reach a definitive diagnosis in athletes showing signs/symptoms, even borderline, of inherited cardiomyopathy/ channelopathy, and in athletes presenting family history of SCD and/or of hereditary cardiac disease. In this review, we revised the molecular basis of the major cardiac diseases associated to sudden cardiac death and the clinical molecular biology approach that can be used to perform risk assessment at DNA level of sudden cardiac death, contributing to the early implementation of adequate therapy. Alterations can occur in ion channel genes, in genes encoding desmosomal and junctional proteins, sarcomeric and Z-disc proteins, proteins for the cytoskeleton and the nuclear envelope. The advent of next generation sequencing (NGS) technology has provided the means to search for mutations in all these genes, at the same time. Therefore, this molecular approach should be the preferred methodology for the aforementioned purpose.
{"title":"Sudden cardiac death in young athletes: Literature review of molecular basis","authors":"C. Mazzaccara, Bruno Mirra, Ferdinando Barretta, B. Lombardo, O. Scudiero, G. Frisso","doi":"10.4081/cardiogenetics.2020.8860","DOIUrl":"https://doi.org/10.4081/cardiogenetics.2020.8860","url":null,"abstract":"Intense athletic training and competition can rarely result in sudden cardiac death (SCD). Despite the introduction of pre-participation cardiovascular screening, especially among young competitive athletes, sport-related SCD remains a debated issue among medical personnel, sports communities and laypersons alike, and generates significant media attention. The most frequent cause of SCD is a hidden inherited cardiomyopathy, the athletes may not even be aware of. Predictive medicine, by searching the presence of pathogenic alterations in cardiac genes, may be an integrative tool, besides the conventional ones used in cardiology (mainly electro and echocardiogram), to reach a definitive diagnosis in athletes showing signs/symptoms, even borderline, of inherited cardiomyopathy/ channelopathy, and in athletes presenting family history of SCD and/or of hereditary cardiac disease. In this review, we revised the molecular basis of the major cardiac diseases associated to sudden cardiac death and the clinical molecular biology approach that can be used to perform risk assessment at DNA level of sudden cardiac death, contributing to the early implementation of adequate therapy. Alterations can occur in ion channel genes, in genes encoding desmosomal and junctional proteins, sarcomeric and Z-disc proteins, proteins for the cytoskeleton and the nuclear envelope. The advent of next generation sequencing (NGS) technology has provided the means to search for mutations in all these genes, at the same time. Therefore, this molecular approach should be the preferred methodology for the aforementioned purpose.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2020-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/cardiogenetics.2020.8860","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42968584","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}
Pub Date : 2019-07-12DOI: 10.4081/CARDIOGENETICS.2019.8194
S. Figliozzi, A. Zorzi, M. P. Marra, A. Ruocco, S. Iliceto, D. Corrado, C. Calore
Kearns-Sayre Syndrome (KSS) is a rare, mitochondrial disease in which cardiac involvement has been associated with poor prognosis. Although the most common clinical manifestation is progressive conduction system impairment, patients can suffer from ventricular arrhythmias. Yet, they show a high prevalence of sudden cardiac death, whose etiopathological mechanism is not completely understood. Cardiac magnetic resonance (CMR) is a rising tool to detect subclinical heart involvement in many heart diseases and was recently able to detect non-ischemic scar in patients affected by KSS. We present a case of a 44 years old patient affected by KSS with a long-standing history of ventricular arrhythmias. Despite electrocardiogram and echocardiogram were normal, CMR showed non-ischemic myocardial scar in the basal-mid lateral wall. Ventricular ectopic beats were assumed to origin from this site, according to their morphology. Our case highlights non-ischemic myocardial scar as a possible etiopathological mechanism of ventricular arrhythmias in patients with KSS. The added value of CMR to provide cardiac involvement identification and risk stratification of these patients is also shown.
{"title":"Non-ischemic scar underlines ventricular arrhythmias in Kearns-Sayre Syndrome.","authors":"S. Figliozzi, A. Zorzi, M. P. Marra, A. Ruocco, S. Iliceto, D. Corrado, C. Calore","doi":"10.4081/CARDIOGENETICS.2019.8194","DOIUrl":"https://doi.org/10.4081/CARDIOGENETICS.2019.8194","url":null,"abstract":"Kearns-Sayre Syndrome (KSS) is a rare, mitochondrial disease in which cardiac involvement has been associated with poor prognosis. Although the most common clinical manifestation is progressive conduction system impairment, patients can suffer from ventricular arrhythmias. Yet, they show a high prevalence of sudden cardiac death, whose etiopathological mechanism is not completely understood. Cardiac magnetic resonance (CMR) is a rising tool to detect subclinical heart involvement in many heart diseases and was recently able to detect non-ischemic scar in patients affected by KSS. \u0000 \u0000We present a case of a 44 years old patient affected by KSS with a long-standing history of ventricular arrhythmias. Despite electrocardiogram and echocardiogram were normal, CMR showed non-ischemic myocardial scar in the basal-mid lateral wall. Ventricular ectopic beats were assumed to origin from this site, according to their morphology. \u0000Our case highlights non-ischemic myocardial scar as a possible etiopathological mechanism of ventricular arrhythmias in patients with KSS. The added value of CMR to provide cardiac involvement identification and risk stratification of these patients is also shown.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/CARDIOGENETICS.2019.8194","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44113456","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}
Pub Date : 2019-06-14DOI: 10.4081/CARDIOGENETICS.2019.7503
P. Hill
Please contact me if this is required.
如果需要，请联系我。
{"title":"An Unusual Cause of Right Heart Failure","authors":"P. Hill","doi":"10.4081/CARDIOGENETICS.2019.7503","DOIUrl":"https://doi.org/10.4081/CARDIOGENETICS.2019.7503","url":null,"abstract":"Please contact me if this is required.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":"1 1","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-06-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/CARDIOGENETICS.2019.7503","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43157524","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}
Pub Date : 2019-04-24DOI: 10.4081/CARDIOGENETICS.2019.7951
J. Skinner
The review article in this journal by Norrish and Kaski focuses on risk of sudden cardiac death in childhood hypertrophic cardiomyopathy and declare it is time to solve the mystery [...]
{"title":"Risk Stratification in Hypertrophic Cardiomyopathy: Time to Think about the Electrocardiogram","authors":"J. Skinner","doi":"10.4081/CARDIOGENETICS.2019.7951","DOIUrl":"https://doi.org/10.4081/CARDIOGENETICS.2019.7951","url":null,"abstract":"The review article in this journal by Norrish and Kaski focuses on risk of sudden cardiac death in childhood hypertrophic cardiomyopathy and declare it is time to solve the mystery [...]","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47592776","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}
Pub Date : 2019-04-24DOI: 10.4081/CARDIOGENETICS.2019.8048
J. Kaski
We thank Prof Skinner for his thoughtful comments on our review article in this Journal. [...]
我们感谢斯金纳教授对我们在《华尔街日报》上发表的评论文章发表的深思熟虑的评论。[…]
{"title":"Response to Skinner: Risk Stratification in Hypertrophic Cardiomyopathy: Time to Think about the Electrocardiogram","authors":"J. Kaski","doi":"10.4081/CARDIOGENETICS.2019.8048","DOIUrl":"https://doi.org/10.4081/CARDIOGENETICS.2019.8048","url":null,"abstract":"We thank Prof Skinner for his thoughtful comments on our review article in this Journal. [...]","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47958497","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}
Pub Date : 2019-04-17DOI: 10.4081/CARDIOGENETICS.2019.7779
G. Limongelli, F. Fratta, A. Cirillo, A. Fusco, Tommaso Marrazzo, Stefania Tramonte, M. Caiazza, G. Caianiello, M. Russo
We report the case of a 15 years old girl with Williams-Beuren syndrome and atrial mixoma.
我们报告了一例15岁女孩，患有Williams-Beuren综合征和心房混合瘤。
{"title":"Atrial Myxoma and Williams-Beuren Syndrome. An Incidental Association?","authors":"G. Limongelli, F. Fratta, A. Cirillo, A. Fusco, Tommaso Marrazzo, Stefania Tramonte, M. Caiazza, G. Caianiello, M. Russo","doi":"10.4081/CARDIOGENETICS.2019.7779","DOIUrl":"https://doi.org/10.4081/CARDIOGENETICS.2019.7779","url":null,"abstract":"We report the case of a 15 years old girl with Williams-Beuren syndrome and atrial mixoma.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":" ","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"44574895","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}
Pub Date : 2019-01-01DOI: 10.4081/cardiogenetics.2019.8181
J. Waning, Y. Hoedemaekers, W. T. Rijdt, Arne I. Jpma, D. Heijsman, K. Caliskan, E. Hoendermis, T. Willems, A. Wijngaard, A. Suurmeijer, M. V. Slegtenhorst, J. Jongbloed, D. Majoor-Krakauer, P. A. Zwaag
The majority of familial noncompaction cardiomyopathy (NCCM) is explained by pathogenic variants in the same sarcomeric genes that are associated with hypertrophic (HCM) and dilated (DCM) cardiomyopathy. Pathogenic variants in the filamin C gene (FLNC) have been linked to HCM and DCM. We expand the spectrum of FLNC related cardiomyopathies by presenting two families with likely pathogenic FLNC variants showing familial segregation of NCCM and concurrent coarctation of the aorta and/or mitral valve abnormalities.
{"title":"FLNC missense variants in familial noncompaction cardiomyopathy","authors":"J. Waning, Y. Hoedemaekers, W. T. Rijdt, Arne I. Jpma, D. Heijsman, K. Caliskan, E. Hoendermis, T. Willems, A. Wijngaard, A. Suurmeijer, M. V. Slegtenhorst, J. Jongbloed, D. Majoor-Krakauer, P. A. Zwaag","doi":"10.4081/cardiogenetics.2019.8181","DOIUrl":"https://doi.org/10.4081/cardiogenetics.2019.8181","url":null,"abstract":"The majority of familial noncompaction cardiomyopathy (NCCM) is explained by pathogenic variants in the same sarcomeric genes that are associated with hypertrophic (HCM) and dilated (DCM) cardiomyopathy. Pathogenic variants in the filamin C gene (FLNC) have been linked to HCM and DCM. We expand the spectrum of FLNC related cardiomyopathies by presenting two families with likely pathogenic FLNC variants showing familial segregation of NCCM and concurrent coarctation of the aorta and/or mitral valve abnormalities.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":"1 1","pages":""},"PeriodicalIF":0.6,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/cardiogenetics.2019.8181","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"70147087","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}
Pub Date : 2018-10-02DOI: 10.4081/cardiogenetics.2018.7671
Leo Kilian, P. Haaf, O. Pfister, A. Vischer, O. Lapaire, T. Burkard
Predominant causes for newly diagnosed postpartum heart failure are preeclampsia and peripartum cardiomyopathy. Being an anatomical variant of Takotsubo syndrome (TTS) reverse TTS in this period is rare. We present a 36 year old patient, who had delivered triplets by cesarean section. Because of postpartum bleeding she was administered sulprostone. Later she was transferred to the Intensive Care Unit with sudden development of dyspnea, tachypnea and tachycardia. Clinical symptoms, laboratory findings and chest radiograph showed signs of acute heart failure. Transthoracic echocardiography (TTE) revealed reverse TTS with moderately reduced left ventricular ejection fraction (LVEF 39%). The patient stabilized with loop diuretic, angiotensine-converting enzyme inhibitors and beta-blockade. Breast-feeding was discouraged and bromocriptine administered. Left ventricular function normalized (LVEF 60%) within four weeks. TTS should be considered in patients with early postpartum development of heart failure. Rapid cardiac recompensation after the start of adequate therapy and complete resolution of clinical symptoms and TTE findings are typical for postpartum TTS.
{"title":"Reverse Takotsubo syndrome, a case report of a rare cause for postpartum heart failure","authors":"Leo Kilian, P. Haaf, O. Pfister, A. Vischer, O. Lapaire, T. Burkard","doi":"10.4081/cardiogenetics.2018.7671","DOIUrl":"https://doi.org/10.4081/cardiogenetics.2018.7671","url":null,"abstract":"Predominant causes for newly diagnosed postpartum heart failure are preeclampsia and peripartum cardiomyopathy. Being an anatomical variant of Takotsubo syndrome (TTS) reverse TTS in this period is rare. We present a 36 year old patient, who had delivered triplets by cesarean section. Because of postpartum bleeding she was administered sulprostone. Later she was transferred to the Intensive Care Unit with sudden development of dyspnea, tachypnea and tachycardia. Clinical symptoms, laboratory findings and chest radiograph showed signs of acute heart failure. Transthoracic echocardiography (TTE) revealed reverse TTS with moderately reduced left ventricular ejection fraction (LVEF 39%). The patient stabilized with loop diuretic, angiotensine-converting enzyme inhibitors and beta-blockade. Breast-feeding was discouraged and bromocriptine administered. Left ventricular function normalized (LVEF 60%) within four weeks. TTS should be considered in patients with early postpartum development of heart failure. Rapid cardiac recompensation after the start of adequate therapy and complete resolution of clinical symptoms and TTE findings are typical for postpartum TTS.","PeriodicalId":41330,"journal":{"name":"Cardiogenetics","volume":"1 1","pages":""},"PeriodicalIF":0.6,"publicationDate":"2018-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.4081/cardiogenetics.2018.7671","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"42813883","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：