Pub Date : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.009
Melanie L. Bozzay, Lan Jiang, A. Zullo, M. Riester, Jacob A Lafo, Zachary J. Kunicki, J. Rudolph, Caroline Madrigal, R. Clements, S. Erqou, Wen-Chih Wu, Stephen Correia, Jennifer M. Primack
prior healthcare utilization, test results, claims data, and mortality.
先前的医疗保健利用、测试结果、索赔数据和死亡率。
{"title":"Mortality in patients with heart failure and suicidal ideation discharged to skilled nursing facilities","authors":"Melanie L. Bozzay, Lan Jiang, A. Zullo, M. Riester, Jacob A Lafo, Zachary J. Kunicki, J. Rudolph, Caroline Madrigal, R. Clements, S. Erqou, Wen-Chih Wu, Stephen Correia, Jennifer M. Primack","doi":"10.11909/j.issn.1671-5411.2022.03.009","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.009","url":null,"abstract":"prior healthcare utilization, test results, claims data, and mortality.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"23 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123422902","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 : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.007
T. Hatab, Mohamad Bahij Moumneh, A. Akkawi, Mohamad Ghazal, S. Alam, M. Refaat
T he coronavirus first reported in China in November 2002 in the form of atypical pneumonia known as the severe acute respiratory syndrome (SARS). The virus then appeared in 2012 in Saudi Arabia as the Middle East respiratory syndrome (MERS). The year 2020 witnessed a novel β-coronavirus related to the previous detected viruses. It was the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — a positive single stranded RNA virus. It was suspected that bats were the main reservoir, leading to speculation about possible animal to human transmission. The ongoing COVID-19 pandemic caused by SARSCoV-2 has already infected over 450 million people worldwide and has killed more than 6 millions. The pandemic strained the emergency medical services in many countries and led to an increased mortality. Researchers stated that the virus can spread from large respiratory droplets on contaminated surfaces, aerosol transmission of small respiratory droplets and from symptomatic, asymptomatic and presymptomatic patients. The WHO declared the COVID-19 as a pandemic on March 11, 2020. Coronaviruses are named after the spikes on their surface which form a crownlike dome, and they are known to cause respiratory infections in humans and animals. SARS-CoV-2, in particular, clinical pattern progresses from an early infection (Stage I), pulmonary phase (Stage II) to hyperinflammation (Stage III) and can be lethal. This has created multiple challenges since acute respiratory infections are one of the known triggers for cardiovascular diseases (CVD), and the presence of CVD may complicate and worsen the course of the infectious disease. COVID-19 binds via its spike protein the Spike protein receptor-binding domain to the zinc peptidase angiotensin-converting enzyme 2 (ACE2), which acts as a receptor for the virus. ACE2 is a surface molecule found on vascular endothelial cells, arterial smooth muscle, and cardiac myocytes. When COVID-19 attaches to ACE2 receptors on myocardial cells, it causes their down regulation as well as imbalance of Angiotensin II (AII) and Angiotensin 1-7 (A1-7) which is generated by ACE2; unbalanced AII activity leads to endothelial injury, inflammation exacerbation and known thrombotic consequences seen in COVID-19 in addition to the inflammatory pathways provoked by lung viral invasion. It is well established that COVID-19 has many systemic and respiratory manifestations, including major severe cardiovascular consequences. COVID19 has been shown to cause myocarditis, type 1 myocardial infarction (acute coronary syndrome and spontaneous coronary artery dissection), type 2 myocardial infarction, arrhythmias, micro-angiopathy, disseminated intravascular coagulation, systemic infection and cytokine storm.
{"title":"COVID-19: cardiovascular manifestations—a review of the cardiac effects","authors":"T. Hatab, Mohamad Bahij Moumneh, A. Akkawi, Mohamad Ghazal, S. Alam, M. Refaat","doi":"10.11909/j.issn.1671-5411.2022.03.007","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.007","url":null,"abstract":"T he coronavirus first reported in China in November 2002 in the form of atypical pneumonia known as the severe acute respiratory syndrome (SARS). The virus then appeared in 2012 in Saudi Arabia as the Middle East respiratory syndrome (MERS). The year 2020 witnessed a novel β-coronavirus related to the previous detected viruses. It was the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — a positive single stranded RNA virus. It was suspected that bats were the main reservoir, leading to speculation about possible animal to human transmission. The ongoing COVID-19 pandemic caused by SARSCoV-2 has already infected over 450 million people worldwide and has killed more than 6 millions. The pandemic strained the emergency medical services in many countries and led to an increased mortality. Researchers stated that the virus can spread from large respiratory droplets on contaminated surfaces, aerosol transmission of small respiratory droplets and from symptomatic, asymptomatic and presymptomatic patients. The WHO declared the COVID-19 as a pandemic on March 11, 2020. Coronaviruses are named after the spikes on their surface which form a crownlike dome, and they are known to cause respiratory infections in humans and animals. SARS-CoV-2, in particular, clinical pattern progresses from an early infection (Stage I), pulmonary phase (Stage II) to hyperinflammation (Stage III) and can be lethal. This has created multiple challenges since acute respiratory infections are one of the known triggers for cardiovascular diseases (CVD), and the presence of CVD may complicate and worsen the course of the infectious disease. COVID-19 binds via its spike protein the Spike protein receptor-binding domain to the zinc peptidase angiotensin-converting enzyme 2 (ACE2), which acts as a receptor for the virus. ACE2 is a surface molecule found on vascular endothelial cells, arterial smooth muscle, and cardiac myocytes. When COVID-19 attaches to ACE2 receptors on myocardial cells, it causes their down regulation as well as imbalance of Angiotensin II (AII) and Angiotensin 1-7 (A1-7) which is generated by ACE2; unbalanced AII activity leads to endothelial injury, inflammation exacerbation and known thrombotic consequences seen in COVID-19 in addition to the inflammatory pathways provoked by lung viral invasion. It is well established that COVID-19 has many systemic and respiratory manifestations, including major severe cardiovascular consequences. COVID19 has been shown to cause myocarditis, type 1 myocardial infarction (acute coronary syndrome and spontaneous coronary artery dissection), type 2 myocardial infarction, arrhythmias, micro-angiopathy, disseminated intravascular coagulation, systemic infection and cytokine storm.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"26 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"129120671","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 : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.001
Akihiro Sakuyama, Masakazu Saitoh, Kentaro Hori, Y. Adachi, K. Iwai, M. Nagayama
OBJECTIVES To investigate the effect of hospital-acquired disability (HAD) on all-cause mortality after discharge according to the body mass index (BMI) in older patients with acute decompensated heart failure. METHODS We included 408 patients aged ≥ 65 years who were hospitalized for acute decompensated heart failure and had undergone an acute phase of cardiac rehabilitation at the Sakakibara Heart Institute between April 2013 and September 2015 (median age: 82 years, interquartile range (IQR): 76–86; 52% male). Patients were divided into three groups based on BMI at hospital admission: underweight (< 18.5 kg/m2), normal weight (18.5 to 25 kg/m2), and overweight (≥ 25 kg/m2). HAD was defined as a decrease of at least five points at discharge compared to before hospitalization according to the Barthel Index. RESULTS The median follow-up period was 475 (IQR: 292–730) days, and all-cause mortality during the follow-up period was 84 deaths (21%). According to multivariate Cox regression analysis, being underweight (HR: 1.941, 95% CI: 1.134−3.321,P = 0.016) or overweight (HR: 0.371, 95% CI: 0.171−0.803,P = 0.012), with normal BMI as the reference, and HAD (HR: 1.857, 95% CI: 1.062−3.250,P = 0.030) were independently associated with all-cause mortality. Patients with HAD exhibited a significantly lower cumulative survival rate in the underweight group (P = 0.001) and tended to have a lower cumulative survival rate in the normal weight group (P = 0.072). HAD was not significantly associated with cumulative survival in the overweight group (P = 0.392). CONCLUSIONS BMI and HAD independently predicted all-cause mortality after discharge in older patients with acute decompensated heart failure. Furthermore, HAD was significantly associated with higher all-cause mortality after discharge, especially in the underweight group.
{"title":"Associations of body mass index and hospital-acquired disability with post-discharge mortality in older patients with acute heart failure","authors":"Akihiro Sakuyama, Masakazu Saitoh, Kentaro Hori, Y. Adachi, K. Iwai, M. Nagayama","doi":"10.11909/j.issn.1671-5411.2022.03.001","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.001","url":null,"abstract":"OBJECTIVES To investigate the effect of hospital-acquired disability (HAD) on all-cause mortality after discharge according to the body mass index (BMI) in older patients with acute decompensated heart failure. METHODS We included 408 patients aged ≥ 65 years who were hospitalized for acute decompensated heart failure and had undergone an acute phase of cardiac rehabilitation at the Sakakibara Heart Institute between April 2013 and September 2015 (median age: 82 years, interquartile range (IQR): 76–86; 52% male). Patients were divided into three groups based on BMI at hospital admission: underweight (< 18.5 kg/m2), normal weight (18.5 to 25 kg/m2), and overweight (≥ 25 kg/m2). HAD was defined as a decrease of at least five points at discharge compared to before hospitalization according to the Barthel Index. RESULTS The median follow-up period was 475 (IQR: 292–730) days, and all-cause mortality during the follow-up period was 84 deaths (21%). According to multivariate Cox regression analysis, being underweight (HR: 1.941, 95% CI: 1.134−3.321,P = 0.016) or overweight (HR: 0.371, 95% CI: 0.171−0.803,P = 0.012), with normal BMI as the reference, and HAD (HR: 1.857, 95% CI: 1.062−3.250,P = 0.030) were independently associated with all-cause mortality. Patients with HAD exhibited a significantly lower cumulative survival rate in the underweight group (P = 0.001) and tended to have a lower cumulative survival rate in the normal weight group (P = 0.072). HAD was not significantly associated with cumulative survival in the overweight group (P = 0.392). CONCLUSIONS BMI and HAD independently predicted all-cause mortality after discharge in older patients with acute decompensated heart failure. Furthermore, HAD was significantly associated with higher all-cause mortality after discharge, especially in the underweight group.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"10 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132592245","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 : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.006
Xuerong Sun, Chendi Cheng, Bin Zhou, Shuang Zhao, Keping Chen, W. Hua, Yangang Su, Wei Xu, Fang-zheng Wang, Xiaohan Fan, Yan Dai, Zhiming Liu, Shu Zhang
OBJECTIVE To evaluate the association of longitudinal changes in physical activity (PA) with long-term outcomes after implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D) implantation. METHODS Patients with ICD/CRT-D implantation from SUMMIT registry were retrospectively analyzed. Accelerometer-derived PA changes over 12 months post implantation were obtained from the archived home monitoring data. The primary endpoints were cardiac death and all-cause mortality. The secondary endpoints were the first ventricular arrthymia (VA) and first appropriate ICD shock. RESULTS In 705 patients, 446 (63.3%) patients showed improved PA over 12 months after implantation. During a mean 61.5-month follow-up duration, 99 cardiac deaths (14.0%) and 153 all-cause deaths (21.7%) occurred. Compared to reduced/unchanged PA, improved PA over 12 months could result in significantly reduced risks of cardiac death (improved PA ≤ 30 min: hazard ratio (HR) = 0.494, 95% CI: 0.288−0.848; > 30 min: HR = 0.390, 95% CI: 0.235−0.648) and all-cause mortality (improved PA ≤ 30 min: HR = 0.467, 95%CI: 0.299−0.728; > 30 min: HR = 0.451, 95% CI: 0.304−0.669). No differences in the VAs or ICD shocks were observed across different groups of PA changes. PA changes can predict the risks of cardiac death only in the low baseline PA group, but improved PA was associated with 56.7%, 57.4%, and 62.3% reduced risks of all-cause mortality in the low, moderate, and high baseline PA groups, respectively, than reduced/unchanged PA. CONCLUSIONS Improved PA could protect aganist cardiac death and all-cause mortality, probably reflecting better clinical efficacy after ICD/CRT-D implantation. Low-intensity exercise training might be encouraged among patients with different baseline PA levels.
{"title":"Association of time-varying changes in physical activity with cardiac death and all-cause mortality after ICD or CRT-D implantation","authors":"Xuerong Sun, Chendi Cheng, Bin Zhou, Shuang Zhao, Keping Chen, W. Hua, Yangang Su, Wei Xu, Fang-zheng Wang, Xiaohan Fan, Yan Dai, Zhiming Liu, Shu Zhang","doi":"10.11909/j.issn.1671-5411.2022.03.006","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.006","url":null,"abstract":"OBJECTIVE To evaluate the association of longitudinal changes in physical activity (PA) with long-term outcomes after implantable cardioverter-defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D) implantation. METHODS Patients with ICD/CRT-D implantation from SUMMIT registry were retrospectively analyzed. Accelerometer-derived PA changes over 12 months post implantation were obtained from the archived home monitoring data. The primary endpoints were cardiac death and all-cause mortality. The secondary endpoints were the first ventricular arrthymia (VA) and first appropriate ICD shock. RESULTS In 705 patients, 446 (63.3%) patients showed improved PA over 12 months after implantation. During a mean 61.5-month follow-up duration, 99 cardiac deaths (14.0%) and 153 all-cause deaths (21.7%) occurred. Compared to reduced/unchanged PA, improved PA over 12 months could result in significantly reduced risks of cardiac death (improved PA ≤ 30 min: hazard ratio (HR) = 0.494, 95% CI: 0.288−0.848; > 30 min: HR = 0.390, 95% CI: 0.235−0.648) and all-cause mortality (improved PA ≤ 30 min: HR = 0.467, 95%CI: 0.299−0.728; > 30 min: HR = 0.451, 95% CI: 0.304−0.669). No differences in the VAs or ICD shocks were observed across different groups of PA changes. PA changes can predict the risks of cardiac death only in the low baseline PA group, but improved PA was associated with 56.7%, 57.4%, and 62.3% reduced risks of all-cause mortality in the low, moderate, and high baseline PA groups, respectively, than reduced/unchanged PA. CONCLUSIONS Improved PA could protect aganist cardiac death and all-cause mortality, probably reflecting better clinical efficacy after ICD/CRT-D implantation. Low-intensity exercise training might be encouraged among patients with different baseline PA levels.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"30 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125187106","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 : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.005
Ying‐Chang Tung, Fu-Chih Hsiao, Chia-Pin Lin, W. Hsu, Pao-Hsien Chu
BACKGROUND Cognitive impairment (CI) is common in patients with heart failure (HF), but the association between CI and biomarkers related to HF or cognitive decline in patients with HF remains unclear. METHODS This prospective observational study investigated the incidence of CI, subsequent cognitive changes, and the association between CI and novel biomarkers in patients with left ventricular ejection fraction < 40% who were hospitalized for acute decompensated HF. Patients were evaluated for CI, depressive symptoms, and quality of life with the Mini-Mental State Examination (MMSE) and the Mini-Cog, Beck Depression Inventory (BDI)-II, and Kansas City Cardiomyopathy Questionnaire (KCCQ), respectively. The primary endpoint was a composite of all-cause mortality or hospitalization for HF at one year. RESULTS Among the 145 patients enrolled in this study, 54 had CI (37.2%) at baseline. The mean MMSE increased significantly at the 3-month and 1-year follow-up, accompanied by decreased BDI-II and increased KCCQ scores. The improvement in the MMSE scores mainly occurred in patients with CI. Among the biomarkers assayed, only growth/differentiation factor (GDF)-15 > 1621.1 pg/mL was significantly associated with CI (area under the curve = 0.64; P = 0.003). An increase in GDF-15 per 1000 units was associated with an increased risk of the primary endpoint (hazard ratio = 1.42; 95% confidence interval: 1.17–1.73; P < 0.001). CONCLUSIONS In patients with HF with CI, cognitive function, depression, and quality of life measures improved at the 3-month and 1-year follow-up. GDF-15 predicted CI with moderate discrimination capacity and was associated with worse HF outcomes.
{"title":"Cognitive impairment and its association with circulating biomarkers in patients with acute decompensated heart failure","authors":"Ying‐Chang Tung, Fu-Chih Hsiao, Chia-Pin Lin, W. Hsu, Pao-Hsien Chu","doi":"10.11909/j.issn.1671-5411.2022.03.005","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.005","url":null,"abstract":"BACKGROUND Cognitive impairment (CI) is common in patients with heart failure (HF), but the association between CI and biomarkers related to HF or cognitive decline in patients with HF remains unclear. METHODS This prospective observational study investigated the incidence of CI, subsequent cognitive changes, and the association between CI and novel biomarkers in patients with left ventricular ejection fraction < 40% who were hospitalized for acute decompensated HF. Patients were evaluated for CI, depressive symptoms, and quality of life with the Mini-Mental State Examination (MMSE) and the Mini-Cog, Beck Depression Inventory (BDI)-II, and Kansas City Cardiomyopathy Questionnaire (KCCQ), respectively. The primary endpoint was a composite of all-cause mortality or hospitalization for HF at one year. RESULTS Among the 145 patients enrolled in this study, 54 had CI (37.2%) at baseline. The mean MMSE increased significantly at the 3-month and 1-year follow-up, accompanied by decreased BDI-II and increased KCCQ scores. The improvement in the MMSE scores mainly occurred in patients with CI. Among the biomarkers assayed, only growth/differentiation factor (GDF)-15 > 1621.1 pg/mL was significantly associated with CI (area under the curve = 0.64; P = 0.003). An increase in GDF-15 per 1000 units was associated with an increased risk of the primary endpoint (hazard ratio = 1.42; 95% confidence interval: 1.17–1.73; P < 0.001). CONCLUSIONS In patients with HF with CI, cognitive function, depression, and quality of life measures improved at the 3-month and 1-year follow-up. GDF-15 predicted CI with moderate discrimination capacity and was associated with worse HF outcomes.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"08 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115426704","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 : 2022-03-28DOI: 10.11909/j.issn.1671-5411.2022.03.003
S. Nuthulaganti, Bijal R Patel, Carly A Rabinowitz, M. Gutierrez, Khadeeja Esmail, R. Omman
C aseous calcification of the mitral annulus (CCMA) is a chronic degenerative process affecting the mitral valve fibrous ring. It is a rare variant of mitral annular calcification (MAC) that is frequently misdiagnosed as endocarditis, cardiac tumor, or abscess. Patients can present with palpitations and dyspnea; however, CCMA does not have a specific clinical presentation and diagnosis is typically made incidentally by presence of an intracardiac mass on cardiac imaging. Transthoracic echocardiography (TTE) remains the preferred imaging modality for diagnosis of CCMA; however, multimodality imaging with transesophageal echocardiography (TEE), cardiac computed tomography (CT), or cardiac MRI (CMRI) may be necessary when the diagnosis remains unclear. Although CCMA is frequently benign, it has been associated with cerebral embolization and valvular dysfunction. Multimodality imaging can clearly differentiate CCMA from other lesions and should be employed when diagnosis remains unclear. Uncomplicated CCMA can be managed conservatively and surgical intervention with mitral valve replacement is reserved for complicated cases. Calcifications of the mitral valve annulus have a higher prevalence in patients with multiple cardiovascular risk factors, as was seen in our patient. While her symptoms of chronic angina, dizziness, dyspnea, and palpitations were likely due to multivessel coronary artery disease (CAD), evaluation of her symptoms led to incidental discovery of a large mobile cardiac mass with high risk for embolization. This case demonstrates the importance of employing multimodality imaging to accurately diagnose CCMA in a highrisk patient (elderly, female, and multiple CAD risk factors). We present the case of a 68 years old Hispanic female with past medical history hypertension, hyperlipidemia, heart failure with preserved ejection fraction, and diabetes mellitus (DM) who presented to the emergency department with one year history of typical anginal chest pain with radiation to the back, dyspnea on exertion, and occasional nighttime dizziness and palpitations. She had an outpatient stress TTE to evaluate chronic angina which revealed a mobile echoic mass on the posterior mitral valve leaflet concerning for tumor, thrombus, or vegetation. Stress echo was prematurely terminated upon detection of the mass and the patient was instructed to start Coumadin and seek further evaluation in the emergency department. Upon admission, patient’s vital signs were within normal limits; basic labs and cultures obtained to rule out concerns for an infectious process were negative for acute infection. CT chest, however, demonstrated extensive calcification in the area of the mitral of the mitral valve annulus. Cardiology was consulted for a transesophageal echocardiogram to further characterize the mass. TEE revealed a hypermobile 0.7 × 1.0 cm pseudo-pedunculated hyperechogenic structure with areas of central lucency extending from the posterior mitral valve ann
{"title":"Caseous calcification of mitral annulus in the setting of multivessel disease","authors":"S. Nuthulaganti, Bijal R Patel, Carly A Rabinowitz, M. Gutierrez, Khadeeja Esmail, R. Omman","doi":"10.11909/j.issn.1671-5411.2022.03.003","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.03.003","url":null,"abstract":"C aseous calcification of the mitral annulus (CCMA) is a chronic degenerative process affecting the mitral valve fibrous ring. It is a rare variant of mitral annular calcification (MAC) that is frequently misdiagnosed as endocarditis, cardiac tumor, or abscess. Patients can present with palpitations and dyspnea; however, CCMA does not have a specific clinical presentation and diagnosis is typically made incidentally by presence of an intracardiac mass on cardiac imaging. Transthoracic echocardiography (TTE) remains the preferred imaging modality for diagnosis of CCMA; however, multimodality imaging with transesophageal echocardiography (TEE), cardiac computed tomography (CT), or cardiac MRI (CMRI) may be necessary when the diagnosis remains unclear. Although CCMA is frequently benign, it has been associated with cerebral embolization and valvular dysfunction. Multimodality imaging can clearly differentiate CCMA from other lesions and should be employed when diagnosis remains unclear. Uncomplicated CCMA can be managed conservatively and surgical intervention with mitral valve replacement is reserved for complicated cases. Calcifications of the mitral valve annulus have a higher prevalence in patients with multiple cardiovascular risk factors, as was seen in our patient. While her symptoms of chronic angina, dizziness, dyspnea, and palpitations were likely due to multivessel coronary artery disease (CAD), evaluation of her symptoms led to incidental discovery of a large mobile cardiac mass with high risk for embolization. This case demonstrates the importance of employing multimodality imaging to accurately diagnose CCMA in a highrisk patient (elderly, female, and multiple CAD risk factors). We present the case of a 68 years old Hispanic female with past medical history hypertension, hyperlipidemia, heart failure with preserved ejection fraction, and diabetes mellitus (DM) who presented to the emergency department with one year history of typical anginal chest pain with radiation to the back, dyspnea on exertion, and occasional nighttime dizziness and palpitations. She had an outpatient stress TTE to evaluate chronic angina which revealed a mobile echoic mass on the posterior mitral valve leaflet concerning for tumor, thrombus, or vegetation. Stress echo was prematurely terminated upon detection of the mass and the patient was instructed to start Coumadin and seek further evaluation in the emergency department. Upon admission, patient’s vital signs were within normal limits; basic labs and cultures obtained to rule out concerns for an infectious process were negative for acute infection. CT chest, however, demonstrated extensive calcification in the area of the mitral of the mitral valve annulus. Cardiology was consulted for a transesophageal echocardiogram to further characterize the mass. TEE revealed a hypermobile 0.7 × 1.0 cm pseudo-pedunculated hyperechogenic structure with areas of central lucency extending from the posterior mitral valve ann","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"79 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"130416205","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)01560-1
T. Mene-Afejuku, G. Jeyashanmugaraja, M. hoq, O. Ola, Amit J. Shah
{"title":"Determinants of mortality among seniors acutely readmitted for heart failure: racial disparities and clinical correlations.","authors":"T. Mene-Afejuku, G. Jeyashanmugaraja, M. hoq, O. Ola, Amit J. Shah","doi":"10.1016/s0735-1097(22)01560-1","DOIUrl":"https://doi.org/10.1016/s0735-1097(22)01560-1","url":null,"abstract":"","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"24 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":"115434341","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 : 2022-01-28DOI: 10.11909/j.issn.1671-5411.2022.01.007
P. Cepas-Guillen, I. Pascual, Eulogio J. García, P. Jiménez-Quevedo, A. Jurado-Román, T. Benito-González, R. Estévez-Loureiro, Pedro Li, D. Arzamendi, B. Melica, E. I. de Oliveira, P. M. Lorenzo, F. Fernández-Vázquez, G. Galeote, L. Nombela‐Franco, L. Unzue, P. Avanzas, M. Sabaté, X. Freixa
1. Cardiology Department, Cardiovascular Institute (ICCV), Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain; 2. Interventional Cardiology Unit, Hospital Universitario Central de Asturias, Department of Medicine, University of Oviedo, Oviedo, Spain; 3. Servicio de Hemodinámica y Cardiología Intervencionista, HM CIEC-Centro Integral de Enfermedades Cardiovasculares, Hospital Universitario HM Montepríncipe, HM Hospitales, Madrid, Spain; Facultad de Medicina, Universidad CEU San Pablo, Madrid, Spain; 4. Servicio de Hemodinámica y Cardiología Intervencionista, HM CIEC-Centro Integral de Enfermedades Cardiovasculares, Hospital Universitario HM Montepríncipe, HM Hospitales, Madrid, Spain; 5. Cardiology Department, Cardiovascular Institute, Hospital Clínico San Carlos, IdISSC, Madrid, Spain; 6. Division of Interventional Cardiology, University Hospital La Paz, IdiPAZ, CIBER-CV, Madrid, Spain; 7. Department of Cardiology, University Hospital of León, León, Spain; 8. Interventional Cardiology Unit, Hospital Álvaro Cunqueiro, Vigo, Spain; 9. Interventional Cardiology Unit, Hospital Sant Pau i Santa Creu, Barcelona, Spain; 10. Serviço de Cardiologia, Centro Hospitalar de Vila Nova de Gaia/Espinho-EPE, Vila Nova de Gaia, Portugal; 11. Serviço de Cardiologia, Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, Centro Académico Médico de Lisboa, Lisboa, Portugal; 12. Servicio de Cardiología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain ✉ Correspondence to: freixa@clinic.cat https://doi.org/10.11909/j.issn.1671-5411.2022.01.007
西班牙巴塞罗那，巴塞罗那大学，医院诊所，IDIBAPS，心血管研究所（ICCV），心脏科；2.西班牙奥维耶多，奥维耶多大学医学系，阿斯图里亚斯中央大学医院，介入心脏病科；3.西班牙马德里，HM 蒙特普林西比大学医院，HM 医院，HM CIEC-Centro Integral de Enfermedades Cardiovasculares，HM CIEC-Centro Integral de Enfermedades Cardiovasculares，血液动力学和介入心脏病学服务；4.西班牙马德里，CEU 圣巴勃罗大学，医学系；5.西班牙马德里，CEU 圣巴勃罗大学，医学系；6.西班牙马德里，CEU 圣巴勃罗大学，医学系；7.西班牙马德里，CEU 圣巴勃罗大学，医学系；8.西班牙马德里，CEU 圣巴勃罗大学，医学系；9.西班牙马德里，CEU 圣巴勃罗大学，医学系。Servicio de Hemodinámica y Cardiología Intervencionista, HM CIEC-Centro Integral de Enfermedades Cardiovasculares, Hospital Universitario HM Montepríncipe, HM Hospitales, Madrid, Spain; 5. Cardiology Department, Cardiovascular Institute, Hospital Clínico San Carlos, IdISSC, Madrid, Spain; 6.西班牙马德里拉巴斯大学医院介入心脏病学部、IdiPAZ、CIBER-CV； 7. 西班牙莱昂莱昂大学医院心脏病学部； 8. 西班牙维哥阿尔瓦罗-孔凯罗医院介入心脏病学室； 9.9. Serviço de Cardiologia, Centro Hospitalar de Vila Nova de Gaia/Espinhoo-EPE, Vila Nova de Gaia, Portugal; 11. Serviço de Cardiologia, Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, Centro Académico Médico de Lisboa, Lisboa, Portugal; 12. Servicio de Cardiología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain ✉ Correspondence to: freixa@clinic.cat https://doi.org/10.11909/j.issn.1671-5411.2022.01.007
{"title":"Transcatheter mitral valve repair in nonagenarians","authors":"P. Cepas-Guillen, I. Pascual, Eulogio J. García, P. Jiménez-Quevedo, A. Jurado-Román, T. Benito-González, R. Estévez-Loureiro, Pedro Li, D. Arzamendi, B. Melica, E. I. de Oliveira, P. M. Lorenzo, F. Fernández-Vázquez, G. Galeote, L. Nombela‐Franco, L. Unzue, P. Avanzas, M. Sabaté, X. Freixa","doi":"10.11909/j.issn.1671-5411.2022.01.007","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.01.007","url":null,"abstract":"1. Cardiology Department, Cardiovascular Institute (ICCV), Hospital Clinic, IDIBAPS, University of Barcelona, Barcelona, Spain; 2. Interventional Cardiology Unit, Hospital Universitario Central de Asturias, Department of Medicine, University of Oviedo, Oviedo, Spain; 3. Servicio de Hemodinámica y Cardiología Intervencionista, HM CIEC-Centro Integral de Enfermedades Cardiovasculares, Hospital Universitario HM Montepríncipe, HM Hospitales, Madrid, Spain; Facultad de Medicina, Universidad CEU San Pablo, Madrid, Spain; 4. Servicio de Hemodinámica y Cardiología Intervencionista, HM CIEC-Centro Integral de Enfermedades Cardiovasculares, Hospital Universitario HM Montepríncipe, HM Hospitales, Madrid, Spain; 5. Cardiology Department, Cardiovascular Institute, Hospital Clínico San Carlos, IdISSC, Madrid, Spain; 6. Division of Interventional Cardiology, University Hospital La Paz, IdiPAZ, CIBER-CV, Madrid, Spain; 7. Department of Cardiology, University Hospital of León, León, Spain; 8. Interventional Cardiology Unit, Hospital Álvaro Cunqueiro, Vigo, Spain; 9. Interventional Cardiology Unit, Hospital Sant Pau i Santa Creu, Barcelona, Spain; 10. Serviço de Cardiologia, Centro Hospitalar de Vila Nova de Gaia/Espinho-EPE, Vila Nova de Gaia, Portugal; 11. Serviço de Cardiologia, Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, Centro Académico Médico de Lisboa, Lisboa, Portugal; 12. Servicio de Cardiología, Hospital Universitario de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain ✉ Correspondence to: freixa@clinic.cat https://doi.org/10.11909/j.issn.1671-5411.2022.01.007","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"69 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"132046541","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 : 2022-01-28DOI: 10.11909/j.issn.1671-5411.2022.01.006
G. Katona, A. Vereckei
Cardiac resynchronization therapy (CRT) is an evidence-based effective therapy of symptomatic heart failure with reduced ejection fraction refractory to optimal medical treatment associated with intraventricular conduction disturbance, that results in electrical dyssynchrony and further deterioration of systolic ventricular function. However, the non-response rate to CRT is still 20%−40%, which can be decreased by better patient selection. The main determinant of CRT outcome is the presence or absence of significant ventricular dyssynchrony and the ability of the applied CRT technique to eliminate it. The current guidelines recommend the determination of QRS morphology and QRS duration and the measurement of left ventricular ejection fraction for patient selection for CRT. However, QRS morphology and QRS duration are not perfect indicators of electrical dyssynchrony, which is the cause of the not negligible non-response rate to CRT and the missed CRT implantation in a significant number of patients who have the appropriate substrate for CRT. Using imaging modalities, many ventricular dyssynchrony criteria were devised for the detection of mechanical dyssynchrony, but their utility in patient selection for CRT is not yet proven, therefore their use is not recommended for this purpose. Moreover, CRT can eliminate only mechanical dyssynchrony due to underlying electrical dyssynchrony, for this reason ECG has a greater role in the detection of ventricular dyssynchrony than imaging modalities. To improve assessment of electrical dyssynchrony, we devised two novel ECG dyssynchrony criteria, which can estimate interventricular and left ventricular intraventricular dyssynchrony in order to improve patient selection for CRT. Here we discuss the results achieved by the application of these new ECG dyssynchrony criteria, which proved to be useful in predicting the CRT response in patients with nonspecific intraventricular conduction disturbance pattern (the second greatest group of CRT candidates), and the significance of other new ECG dyssynchrony criteria in the potential improvement of CRT outcome.
{"title":"Novel electrocardiographic dyssynchrony criteria that may improve patient selection for cardiac resynchronization therapy","authors":"G. Katona, A. Vereckei","doi":"10.11909/j.issn.1671-5411.2022.01.006","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.01.006","url":null,"abstract":"Cardiac resynchronization therapy (CRT) is an evidence-based effective therapy of symptomatic heart failure with reduced ejection fraction refractory to optimal medical treatment associated with intraventricular conduction disturbance, that results in electrical dyssynchrony and further deterioration of systolic ventricular function. However, the non-response rate to CRT is still 20%−40%, which can be decreased by better patient selection. The main determinant of CRT outcome is the presence or absence of significant ventricular dyssynchrony and the ability of the applied CRT technique to eliminate it. The current guidelines recommend the determination of QRS morphology and QRS duration and the measurement of left ventricular ejection fraction for patient selection for CRT. However, QRS morphology and QRS duration are not perfect indicators of electrical dyssynchrony, which is the cause of the not negligible non-response rate to CRT and the missed CRT implantation in a significant number of patients who have the appropriate substrate for CRT. Using imaging modalities, many ventricular dyssynchrony criteria were devised for the detection of mechanical dyssynchrony, but their utility in patient selection for CRT is not yet proven, therefore their use is not recommended for this purpose. Moreover, CRT can eliminate only mechanical dyssynchrony due to underlying electrical dyssynchrony, for this reason ECG has a greater role in the detection of ventricular dyssynchrony than imaging modalities. To improve assessment of electrical dyssynchrony, we devised two novel ECG dyssynchrony criteria, which can estimate interventricular and left ventricular intraventricular dyssynchrony in order to improve patient selection for CRT. Here we discuss the results achieved by the application of these new ECG dyssynchrony criteria, which proved to be useful in predicting the CRT response in patients with nonspecific intraventricular conduction disturbance pattern (the second greatest group of CRT candidates), and the significance of other new ECG dyssynchrony criteria in the potential improvement of CRT outcome.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"93 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126629663","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 : 2022-01-28DOI: 10.11909/j.issn.1671-5411.2022.01.002
Ying Huang, W. Lai, Hong Chen, Qifang Liu, Ju-xiang Li, Jin-zhu Hu
BACKGROUND As an antioxidant, serum superoxide dismutase (SOD) have been found to be associated with hypertension. METHODS The data were derived from the Chinese Longitudinal Healthy Longevity Survey (CLHLS), a prospective cohort study in China. We explored the association between serum SOD and blood pressure (BP) using multivariable correction analysis in an older Chinese population. RESULTS We observed a significantly gradual downward trend in the association between serum SOD levels and diastolic BP (DBP) in participants with lower serum SOD levels (< 58 IU/mL), while no associations were observed between serum SOD levels and DBP in participants with higher serum SOD levels (> 58 IU/mL). Similar results showed a significant gradual downward trend in associations between serum SOD levels and the risk of diastolic hypertension only at SOD < 58 IU/mL. Multiple linear regression analysis suggested that serum SOD was negatively correlated with DBP (Sβ = —0.088,P < 0.001) but not with SBP (Sβ = 0.013, P = 0.607). Multiple logistic regression analysis suggested that serum SOD was independently associated with the risk of diastolic hypertension (OR = 0.984, 95% CI: 0.973−0.996, P = 0.010) but not with the risk of systolic hypertension (OR = 1.001, 95% CI: 0.990−1.012,P = 0.836)) after adjusting for relevant confounding factors. Serum SOD levels (< 58 IU/mL, > 58 IU/mL) were an effect modifier of the association between serum SOD and DBP (interactionP = 0.0038) or the risk of diastolic hypertension (interaction P = 0.0050). CONCLUSIONS Our study indicated for the first time that there was an L-shaped association between serum SOD levels and the risk of diastolic hypertension in the older Chinese population.
{"title":"The L-shaped association between superoxide dismutase levels and blood pressure in older Chinese adults: community-based, cross-sectional study","authors":"Ying Huang, W. Lai, Hong Chen, Qifang Liu, Ju-xiang Li, Jin-zhu Hu","doi":"10.11909/j.issn.1671-5411.2022.01.002","DOIUrl":"https://doi.org/10.11909/j.issn.1671-5411.2022.01.002","url":null,"abstract":"BACKGROUND As an antioxidant, serum superoxide dismutase (SOD) have been found to be associated with hypertension. METHODS The data were derived from the Chinese Longitudinal Healthy Longevity Survey (CLHLS), a prospective cohort study in China. We explored the association between serum SOD and blood pressure (BP) using multivariable correction analysis in an older Chinese population. RESULTS We observed a significantly gradual downward trend in the association between serum SOD levels and diastolic BP (DBP) in participants with lower serum SOD levels (< 58 IU/mL), while no associations were observed between serum SOD levels and DBP in participants with higher serum SOD levels (> 58 IU/mL). Similar results showed a significant gradual downward trend in associations between serum SOD levels and the risk of diastolic hypertension only at SOD < 58 IU/mL. Multiple linear regression analysis suggested that serum SOD was negatively correlated with DBP (Sβ = —0.088,P < 0.001) but not with SBP (Sβ = 0.013, P = 0.607). Multiple logistic regression analysis suggested that serum SOD was independently associated with the risk of diastolic hypertension (OR = 0.984, 95% CI: 0.973−0.996, P = 0.010) but not with the risk of systolic hypertension (OR = 1.001, 95% CI: 0.990−1.012,P = 0.836)) after adjusting for relevant confounding factors. Serum SOD levels (< 58 IU/mL, > 58 IU/mL) were an effect modifier of the association between serum SOD and DBP (interactionP = 0.0038) or the risk of diastolic hypertension (interaction P = 0.0050). CONCLUSIONS Our study indicated for the first time that there was an L-shaped association between serum SOD levels and the risk of diastolic hypertension in the older Chinese population.","PeriodicalId":285674,"journal":{"name":"Journal of geriatric cardiology : JGC","volume":"25 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115834722","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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