Pub Date : 2023-12-01DOI: 10.1016/j.cjca.2023.11.045
Prem Soman, Abudllah Zoheb Azhar
{"title":"Determining the natural history of a rare disease: A narrow window of opportunity.","authors":"Prem Soman, Abudllah Zoheb Azhar","doi":"10.1016/j.cjca.2023.11.045","DOIUrl":"https://doi.org/10.1016/j.cjca.2023.11.045","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"259 ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139014131","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 : 2023-12-01DOI: 10.1016/j.cjca.2023.12.014
Fernando Rivera-Theurel, Paul Oh, P. Thavendiranathan, Rebecca Laundos, Malak El-Rayes, Natalia Nugaeva, Diego Hernan Delgado
{"title":"EXerCise InTErvention for Patients with Transthyretin Amyloid Cardiomyopathy (EXCITE-ATTR-CM) - Pilot Study.","authors":"Fernando Rivera-Theurel, Paul Oh, P. Thavendiranathan, Rebecca Laundos, Malak El-Rayes, Natalia Nugaeva, Diego Hernan Delgado","doi":"10.1016/j.cjca.2023.12.014","DOIUrl":"https://doi.org/10.1016/j.cjca.2023.12.014","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"40 7","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139024738","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 : 2023-05-19DOI: 10.1101/2023.05.18.23290189
J. Brophy, L. Nadeau
Background: Atrial fibrillation is one of the most common arrhythmias but the optimal drug choice for a rate control strategy remains uncertain. In particular, controversy and uncertainty exists regarding the safety of digoxin in this context. Methods: This was a retrospective cohort claims database study of patients with an incident hospital discharge diagnosis of atrial fibrillation between 2011 and 2015. The exposure variables were a discharge prescription for beta blockers, digoxin or both. The primary outcome was a composite of total in-hospital mortality or a repeat cardiovascular (CV) hospitalization. Secondary outcomes were the individual components of the primary outcome. Baseline confounding was controlled with propensity score inverse probability weighting using a entropy balancing algorithm and the prespecified estimand was the average treatment effect among the treated. In sensitivity analyses, baseline covariate imbalances were adjusted using a maximum likelihood algorithm and an overall average treatment effect estimand. Treatment effects for the weighted samples were calculated from a Cox proportional hazards model. Results: 12,723 patients were discharged on beta blockers alone, 406 on digoxin alone, and 1,499 discharged on combined beta blocker / digoxin therapy with a median follow-up time of 356 days. In the unadjusted analyses, the primary outcome occured most frequently in the combined exposure group (15.5%) compared to the isolated digoxin (13.3%) and beta blocker (11.5%) groups (p < 0.001 for trend). There were more CV hospitalizations in the combined beta blocker / digoxin group (14.4%) compared to the BB (10.7%) or digoxin (10.6%) groups (p = 0.006 for trend). There were more deaths in the digoxin group (2.7%) and the combined group (1.1%) groups compared to the BB alone group (0.8%) (p < 0.001 for trend). However, after baseline covariate adjustment, the digoxin alone (hazard ratio (HR) 1.24, 95% CI 0.85 - 1.81) and the combined group (HR 1.09, 95% CI 0.90 - 1.31) were not associated with increased risk for the composite endpoint compared with the beta blocker alone group. These results were robust to sensitivity analyses. Conclusion: After accounting for baseline imbalances, patients hospitalized for incident atrial fibrillation and discharged on digoxin alone or the combination of digoxin and a beta blocker were not associated with an increase in the composite outcome of recurrent CV hospitalizations and death compared to those discharged on isolated beta blocker therapy. However, additional studies are required to refine the precision of these estimates.
背景:房颤是最常见的心律失常之一，但控制心率的最佳药物选择仍不确定。特别是，在这种情况下，地高辛的安全性存在争议和不确定性。方法:采用回顾性队列索赔数据库研究2011 - 2015年间因房颤意外出院的患者。暴露变量是-受体阻滞剂，地高辛或两者的出院处方。主要结局是住院总死亡率或重复心血管(CV)住院的综合结果。次要结局是主要结局的各个组成部分。使用熵平衡算法用倾向得分逆概率加权控制基线混淆，预先设定的估计值为被治疗组的平均治疗效果。在敏感性分析中，使用最大似然算法和总体平均治疗效果估计来调整基线协变量失衡。加权样本的处理效果通过Cox比例风险模型计算。结果:12723例患者单独使用受体阻滞剂出院，406例单独使用地高辛，1499例患者联合使用受体阻滞剂/地高辛，中位随访时间为356天。在未经调整的分析中，主要结局在联合暴露组(15.5%)比单独地高辛组(13.3%)和受体阻滞剂组(11.5%)发生的频率最高(趋势p < 0.001)。与BB组(10.7%)或地高辛组(10.6%)相比，-受体阻滞剂/地高辛联合组的CV住院率(14.4%)更高(趋势p = 0.006)。地高辛组(2.7%)和联合组(1.1%)的死亡率高于单独使用BB组(0.8%)(趋势p < 0.001)。然而，在基线协变量调整后，与单独使用受体阻滞剂组相比，单独使用地高辛组(风险比1.24,95% CI 0.85 - 1.81)和联合使用地高辛组(风险比1.09,95% CI 0.90 - 1.31)与复合终点的风险增加无关。这些结果对敏感性分析是稳健的。结论:在考虑基线不平衡后，因房颤住院且出院时单独使用地高辛或联合使用地高辛和β受体阻滞剂的患者与单独使用β受体阻滞剂的患者相比，复发性CV住院和死亡的复合结局增加无关。但是，需要进一步的研究来提高这些估计的精确度。
{"title":"Beta blockers, digoxin or both following an incident diagnosis of atrial fibrillation; a prospective cohort study","authors":"J. Brophy, L. Nadeau","doi":"10.1101/2023.05.18.23290189","DOIUrl":"https://doi.org/10.1101/2023.05.18.23290189","url":null,"abstract":"Background: Atrial fibrillation is one of the most common arrhythmias but the optimal drug choice for a rate control strategy remains uncertain. In particular, controversy and uncertainty exists regarding the safety of digoxin in this context. Methods: This was a retrospective cohort claims database study of patients with an incident hospital discharge diagnosis of atrial fibrillation between 2011 and 2015. The exposure variables were a discharge prescription for beta blockers, digoxin or both. The primary outcome was a composite of total in-hospital mortality or a repeat cardiovascular (CV) hospitalization. Secondary outcomes were the individual components of the primary outcome. Baseline confounding was controlled with propensity score inverse probability weighting using a entropy balancing algorithm and the prespecified estimand was the average treatment effect among the treated. In sensitivity analyses, baseline covariate imbalances were adjusted using a maximum likelihood algorithm and an overall average treatment effect estimand. Treatment effects for the weighted samples were calculated from a Cox proportional hazards model. Results: 12,723 patients were discharged on beta blockers alone, 406 on digoxin alone, and 1,499 discharged on combined beta blocker / digoxin therapy with a median follow-up time of 356 days. In the unadjusted analyses, the primary outcome occured most frequently in the combined exposure group (15.5%) compared to the isolated digoxin (13.3%) and beta blocker (11.5%) groups (p < 0.001 for trend). There were more CV hospitalizations in the combined beta blocker / digoxin group (14.4%) compared to the BB (10.7%) or digoxin (10.6%) groups (p = 0.006 for trend). There were more deaths in the digoxin group (2.7%) and the combined group (1.1%) groups compared to the BB alone group (0.8%) (p < 0.001 for trend). However, after baseline covariate adjustment, the digoxin alone (hazard ratio (HR) 1.24, 95% CI 0.85 - 1.81) and the combined group (HR 1.09, 95% CI 0.90 - 1.31) were not associated with increased risk for the composite endpoint compared with the beta blocker alone group. These results were robust to sensitivity analyses. Conclusion: After accounting for baseline imbalances, patients hospitalized for incident atrial fibrillation and discharged on digoxin alone or the combination of digoxin and a beta blocker were not associated with an increase in the composite outcome of recurrent CV hospitalizations and death compared to those discharged on isolated beta blocker therapy. However, additional studies are required to refine the precision of these estimates.","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-05-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130833135","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 : 2023-03-20DOI: 10.1101/2023.03.13.23287209
E. Lecluze, G. Lettre
Background: Hypertension, clinically defined by elevated blood pressure (BP), is an important cause of mortality and morbidity worldwide. Many risk factors for hypertension are known, including a positive family history, which suggests that genetics contribute to inter-individual BP variation. Genome-wide association studies (GWAS) have identified >1000 loci associated with BP, yet the identity of the genes responsible for these associations remains largely unknown. Methods: To pinpoint genes that causally impact BP variation in humans, we analyzed predicted loss-of-function (pLoF) variants in the UK Biobank whole-exome sequencing dataset (n=454,709 participants, 6% non-European ancestry). We analyzed genetic associations between systolic or diastolic BP (SBP/DBP) and single pLoF variants (additive and recessive genetic models) as well as with the burden of very rare pLoF variants (minor allele frequency [MAF] <0.01%). Results: Single pLoF variants in ten genes associated with BP (ANKDD1B, ENPEP, PNCK, BTN3A2, C1orf145 [OBSCN-AS1], CASP9, DBH, KIAA1161 [MYORG], OR4X1, and TMC3). We also found a burden of rare pLoF variants in five additional genes associated with BP (TTN, NOS3, FES, SMAD6, COL21A1). Except for PNCK, which is located on the X-chromosome, these genes map near variants previously associated with BP by GWAS, validating the study of pLoF variants to prioritize causal genes at GWAS loci. Conclusions: Our study highlights 15 genes that likely modulate BP in humans, including five genes that harbor pLoF variants associated with lower BP.
{"title":"Association analyses of predicted loss-of-function variants prioritized 15 genes as blood pressure regulators","authors":"E. Lecluze, G. Lettre","doi":"10.1101/2023.03.13.23287209","DOIUrl":"https://doi.org/10.1101/2023.03.13.23287209","url":null,"abstract":"Background: Hypertension, clinically defined by elevated blood pressure (BP), is an important cause of mortality and morbidity worldwide. Many risk factors for hypertension are known, including a positive family history, which suggests that genetics contribute to inter-individual BP variation. Genome-wide association studies (GWAS) have identified >1000 loci associated with BP, yet the identity of the genes responsible for these associations remains largely unknown. Methods: To pinpoint genes that causally impact BP variation in humans, we analyzed predicted loss-of-function (pLoF) variants in the UK Biobank whole-exome sequencing dataset (n=454,709 participants, 6% non-European ancestry). We analyzed genetic associations between systolic or diastolic BP (SBP/DBP) and single pLoF variants (additive and recessive genetic models) as well as with the burden of very rare pLoF variants (minor allele frequency [MAF] <0.01%). Results: Single pLoF variants in ten genes associated with BP (ANKDD1B, ENPEP, PNCK, BTN3A2, C1orf145 [OBSCN-AS1], CASP9, DBH, KIAA1161 [MYORG], OR4X1, and TMC3). We also found a burden of rare pLoF variants in five additional genes associated with BP (TTN, NOS3, FES, SMAD6, COL21A1). Except for PNCK, which is located on the X-chromosome, these genes map near variants previously associated with BP by GWAS, validating the study of pLoF variants to prioritize causal genes at GWAS loci. Conclusions: Our study highlights 15 genes that likely modulate BP in humans, including five genes that harbor pLoF variants associated with lower BP.","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131319188","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 : 2022-10-01DOI: 10.1016/j.cjca.2022.08.172
K. Bouchard, M. Dans, P. Liu, K. Dautenhahn, M. Ghafurian, J. Fiedorowicz, H. Tulloch
{"title":"THE SOCIAL ROBOTS ARE COMING: HEALTH CARE PROVIDERS' PERSPECTIVES OF SOCIAL ROBOTS AS A FORM OF VIRTUAL CARE IN CARDIOVASCULAR MEDICINE","authors":"K. Bouchard, M. Dans, P. Liu, K. Dautenhahn, M. Ghafurian, J. Fiedorowicz, H. Tulloch","doi":"10.1016/j.cjca.2022.08.172","DOIUrl":"https://doi.org/10.1016/j.cjca.2022.08.172","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"46 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114105983","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 : 2022-10-01DOI: 10.1016/j.cjca.2022.08.210
A. Charlebois, E. Macphee, R. Coulton
{"title":"CARDIAC SURGERY VIRTUAL FOLLOW-UP FOR PATIENTS AT HIGH-RISK FOR HOSPITAL READMISSION: DEVELOPMENT OF AN ENHANCED REMOTE TELEMONITORING CARE PLATFORM","authors":"A. Charlebois, E. Macphee, R. Coulton","doi":"10.1016/j.cjca.2022.08.210","DOIUrl":"https://doi.org/10.1016/j.cjca.2022.08.210","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"30 5 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131492268","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 : 2022-10-01DOI: 10.1016/j.cjca.2022.08.149
R. Teskey
{"title":"COVID-19 RISK IN THE CARDIAC CATHETERIZATION LABORATORY","authors":"R. Teskey","doi":"10.1016/j.cjca.2022.08.149","DOIUrl":"https://doi.org/10.1016/j.cjca.2022.08.149","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"182 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"116652601","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 : 2022-03-01DOI: 10.1016/j.cjca.2022.03.008
Andaç Karadeniz, Erdi Babayiğit, Prof Bülent Görenek
{"title":"Could Branched-Chain Amino Acids Be a New Landmark in Metabolic Syndrome and Cardiac Arrhythmias?","authors":"Andaç Karadeniz, Erdi Babayiğit, Prof Bülent Görenek","doi":"10.1016/j.cjca.2022.03.008","DOIUrl":"https://doi.org/10.1016/j.cjca.2022.03.008","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"8 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"119794004","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 : 2022-03-01DOI: 10.1016/s0735-1097(22)02391-9
A. Egbe, William R. Miranda, Jason H. Anderson, R. Katta, A. Goda, Kartik Andi, P. Kamath, H. Connolly
{"title":"Determinants and Prognostic Implications of Hepatorenal Dysfunction in Adults with Congenital Heart Disease.","authors":"A. Egbe, William R. Miranda, Jason H. Anderson, R. Katta, A. Goda, Kartik Andi, P. Kamath, H. Connolly","doi":"10.1016/s0735-1097(22)02391-9","DOIUrl":"https://doi.org/10.1016/s0735-1097(22)02391-9","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"21 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124035731","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 : 2022-03-01DOI: 10.1016/j.cjca.2022.03.007
L. Verreault-Julien, S. Rinfret
{"title":"Prolonged Reperfusion Delays During the COVID-19 Pandemic: Is Faster Always Better?","authors":"L. Verreault-Julien, S. Rinfret","doi":"10.1016/j.cjca.2022.03.007","DOIUrl":"https://doi.org/10.1016/j.cjca.2022.03.007","url":null,"abstract":"","PeriodicalId":425026,"journal":{"name":"The Canadian journal of cardiology","volume":"15 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120241018","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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