Inotropes historically all increased intra-cellular calcium levels and they commonly caused intracellular Ca2+ overload and triggered malignant arrhythmias. The myosin activators, such as Omecamtiv Mecarbil (OM), increase myosin activity and function, and modify acto-myosin interaction through calcium-independent mechanisms. OM is a selective cardiac myosin activator that binds specifically the catalytic domain of cardiac myosin without any significant effect over other types of non-cardiac myosin. It increases the speed of ATP hydrolysis and, therefore, accelerates the transition rate to a strongly bound force-producing state, increases the number of myosin heads that interact with actin filaments and increases the proportion of time they are in a force producing state. OM decreases the inefficient use of non-contractile energy. OM has been studied in 4 phase II clinical trials with more than 1,300 patients with heart failure. The GALACTIC-HF trial is a nearly 8,000 patient HFrEF mortality/morbidity trial which started recruiting in January 2017 and should be completed soon.
{"title":"Myosin Activators","authors":"G. Rosano, P. Ponikowski","doi":"10.17987/icfj.v18i0.611","DOIUrl":"https://doi.org/10.17987/icfj.v18i0.611","url":null,"abstract":"Inotropes historically all increased intra-cellular calcium levels and they commonly caused intracellular Ca2+ overload and triggered malignant arrhythmias. The myosin activators, such as Omecamtiv Mecarbil (OM), increase myosin activity and function, and modify acto-myosin interaction through calcium-independent mechanisms. OM is a selective cardiac myosin activator that binds specifically the catalytic domain of cardiac myosin without any significant effect over other types of non-cardiac myosin. It increases the speed of ATP hydrolysis and, therefore, accelerates the transition rate to a strongly bound force-producing state, increases the number of myosin heads that interact with actin filaments and increases the proportion of time they are in a force producing state. OM decreases the inefficient use of non-contractile energy. OM has been studied in 4 phase II clinical trials with more than 1,300 patients with heart failure. The GALACTIC-HF trial is a nearly 8,000 patient HFrEF mortality/morbidity trial which started recruiting in January 2017 and should be completed soon.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"95 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79235882","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}
{"title":"Anticoagulants and Antithrombotics","authors":"Justyna Domienik-Karłowicz, Y. Lopatin","doi":"10.17987/icfj.v18i0.619","DOIUrl":"https://doi.org/10.17987/icfj.v18i0.619","url":null,"abstract":"No abstract","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77670522","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}
P. Fountoulakis, A. Siama, A. Kalogeris, M. Iliopoulou, A. Tsoukas, A. Manolis
Fungal endocarditis, a rare and lethal infection, is aetiologically connected with Candida and Aspergillus species. Among these two agents, Candida is a common nosocomial infection with increasing rates over the last years and mortality up to 40% in cases of systemic candidiasis. In the present paper, we describe the case of a 58 year old woman with metastatic breast cancer under palliative chemotherapy who was hospitalized for recurrent episodes of fever due to fungal endocarditis of the implantable venous access port. Such cases may elude the attention of the physician and need to be taken into account especially in oncologic patients with implantable devices under chemotherapy regimens. The treatment of Candida endocarditis can be difficult because of the formation of biofilms on prosthetic devices. The prognosis of these patients may be ameliorated with the combination of fungal and invasive treatment.
{"title":"Tricuspid Valve Fungal Endocarditis in a Patient with Breast Cancer and an Implantable Chemotherapy Venous Access Port","authors":"P. Fountoulakis, A. Siama, A. Kalogeris, M. Iliopoulou, A. Tsoukas, A. Manolis","doi":"10.17987/icfj.v16i0.581","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.581","url":null,"abstract":"Fungal endocarditis, a rare and lethal infection, is aetiologically connected with Candida and Aspergillus species. Among these two agents, Candida is a common nosocomial infection with increasing rates over the last years and mortality up to 40% in cases of systemic candidiasis. In the present paper, we describe the case of a 58 year old woman with metastatic breast cancer under palliative chemotherapy who was hospitalized for recurrent episodes of fever due to fungal endocarditis of the implantable venous access port. Such cases may elude the attention of the physician and need to be taken into account especially in oncologic patients with implantable devices under chemotherapy regimens. The treatment of Candida endocarditis can be difficult because of the formation of biofilms on prosthetic devices. The prognosis of these patients may be ameliorated with the combination of fungal and invasive treatment.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"48 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81401280","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}
Calcific coronary artery disease (CCAD) may cause abnormal myocardial perfusion and hence generalized ischaemia, despite potential discrepancy in its expression pattern compared to the well-known atherosclerotic disease which raises questions about the exact pathophysiology of coronary calcification and whether there is a genetic aetiology for it. In a pilot study we studied three candidate genes, ENPP1, ABCC6 and NTE5 which may predispose to coronary arterial or valvular calcification. We studied 65 patients with CCAD and 5 patients with calcific aortic valve disease (CAVD). Five DNA variants potentially affecting protein function were found in six patients. Our findings support genetic variants might influence the development of CCAD and CAVD, however, segregation in the families must first be performed to ascertain any damaging effect of these variants. The search for direct causative genetic variants in coronary artery and aortic valve calcification must be broadened with other genes.
{"title":"Is there a Role for Genetics in Cardiac Calcification?","authors":"U. Hellman, S. Mörner, M. Henein","doi":"10.17987/icfj.v16i0.587","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.587","url":null,"abstract":"Calcific coronary artery disease (CCAD) may cause abnormal myocardial perfusion and hence generalized ischaemia, despite potential discrepancy in its expression pattern compared to the well-known atherosclerotic disease which raises questions about the exact pathophysiology of coronary calcification and whether there is a genetic aetiology for it. In a pilot study we studied three candidate genes, ENPP1, ABCC6 and NTE5 which may predispose to coronary arterial or valvular calcification. We studied 65 patients with CCAD and 5 patients with calcific aortic valve disease (CAVD). Five DNA variants potentially affecting protein function were found in six patients. Our findings support genetic variants might influence the development of CCAD and CAVD, however, segregation in the families must first be performed to ascertain any damaging effect of these variants. The search for direct causative genetic variants in coronary artery and aortic valve calcification must be broadened with other genes.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73806088","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}
Background Recent case reports of early structural degeneration of the Mitroflow valve have cast doubts on the suitability of this bioprosthesis, particularly in the smaller sizes, and in younger patients. We studied long-term patient survival, in a comparative study, as a marker of success after aortic valve replacement.Methods Long-term survival in 142 consecutive patients implanted with the Mitroflow valve was compared, using the Kaplan-Meier method, with a control group of 149 patients receiving different bioprostheses. Ninety two percent of patients were over 70 and the Mitroflow was used preferentially in smaller sizes.Results Long-term survival in patients who received a Mitroflow valve was equivalent to controls. Four documented cases of premature structural valve degeneration (3 Mitroflow, 1 Perimount) required a second intervention.Conclusions The Mitroflow compared favourably with other valves in our practice. Although a few patients required further treatment this had no significant adverse impact on overall survival.
{"title":"Long-term Survival after Aortic Valve Replacement with the Mitroflow Bioprosthesis: a Comparative Study","authors":"A. Manché, L. Camilleri","doi":"10.17987/icfj.v16i0.533","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.533","url":null,"abstract":"Background Recent case reports of early structural degeneration of the Mitroflow valve have cast doubts on the suitability of this bioprosthesis, particularly in the smaller sizes, and in younger patients. We studied long-term patient survival, in a comparative study, as a marker of success after aortic valve replacement.Methods Long-term survival in 142 consecutive patients implanted with the Mitroflow valve was compared, using the Kaplan-Meier method, with a control group of 149 patients receiving different bioprostheses. Ninety two percent of patients were over 70 and the Mitroflow was used preferentially in smaller sizes.Results Long-term survival in patients who received a Mitroflow valve was equivalent to controls. Four documented cases of premature structural valve degeneration (3 Mitroflow, 1 Perimount) required a second intervention.Conclusions The Mitroflow compared favourably with other valves in our practice. Although a few patients required further treatment this had no significant adverse impact on overall survival.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85857374","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}
BackgroundInfluence of comorbidity on adherence to lifestyle therapy in patients with chronic heart failure (CHF) have not been studied yet.The aimThe aim of this study was to investigate awareness and adherence to lifestyle therapy in patient with CHF and comorbidity.Мethods203 patients with CHF (130 males and 73 females, mean age was 61,8±9,6 years) were studied. CHF was defined according to ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2016. Charlson comorbidity index was calculated. Awareness of lifestyle modifications was determined using a questionnaire developed in our clinic and used in previous scientific studies. Quality of life, psychological state, relation to disease were estimated. Follow-Up period was 1 year.ResultsThe awareness about lifestyle modifications in patients with CHF ranged from 38.9% (daily control of body weight) to 87.2% (reduced intake of dietary sodium). Adherence to lifestyle therapy was from 7.9% (daily weight control) to 37.9% (reduced intake of dietary sodium). Charlson comorbidity index corrected by age was 5.0±2.1 scores. Patients with high comorbidity (Charlson comorbidity index > 6 scores) had decreased of quality of life. There were not differences in adherence to lifestyle therapy in patients with CHF, depending on the level of comorbidity. Nonadherence patients were characterized by sensitive type of relation to disease, emotional lability (p< 0,05).СonclusionNonadherence to lifestyle therapy in patients with CHF is associated with desadaptive type of relation to disease, which is more common in patients with high comorbidity.
{"title":"Adherence to Lifestyle Therapy in Patients with Chronic Heart Failure and Comorbidity","authors":"E. Efremova, A. Shutov","doi":"10.17987/icfj.v16i0.574","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.574","url":null,"abstract":"BackgroundInfluence of comorbidity on adherence to lifestyle therapy in patients with chronic heart failure (CHF) have not been studied yet.The aimThe aim of this study was to investigate awareness and adherence to lifestyle therapy in patient with CHF and comorbidity.Мethods203 patients with CHF (130 males and 73 females, mean age was 61,8±9,6 years) were studied. CHF was defined according to ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure, 2016. Charlson comorbidity index was calculated. Awareness of lifestyle modifications was determined using a questionnaire developed in our clinic and used in previous scientific studies. Quality of life, psychological state, relation to disease were estimated. Follow-Up period was 1 year.ResultsThe awareness about lifestyle modifications in patients with CHF ranged from 38.9% (daily control of body weight) to 87.2% (reduced intake of dietary sodium). Adherence to lifestyle therapy was from 7.9% (daily weight control) to 37.9% (reduced intake of dietary sodium). Charlson comorbidity index corrected by age was 5.0±2.1 scores. Patients with high comorbidity (Charlson comorbidity index > 6 scores) had decreased of quality of life. There were not differences in adherence to lifestyle therapy in patients with CHF, depending on the level of comorbidity. Nonadherence patients were characterized by sensitive type of relation to disease, emotional lability (p< 0,05).СonclusionNonadherence to lifestyle therapy in patients with CHF is associated with desadaptive type of relation to disease, which is more common in patients with high comorbidity.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89379988","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}
We present an interesting case of a middle-aged male patient with recent diagnosis of diffuse large B-cell lymphoma, who underwent a staging CT scan that revealed hypoattenuated lesions in the right atrium initially suspicious of thrombi. They were not evidence on transthoracic echocardiography, but the transesophageal echocardiogram showed a large mobile mass infiltrating and extending the right atrium, interatrial septum and aortic root. This case further illustrates the excellent sensitivity and specificity of transesophageal echocardiography for intracardiac masses but also the importance of multimodality cardiac imaging to reach a diagnosis and guide management.
{"title":"What’s that in the right atrium?","authors":"T. Wang, N. Pelt","doi":"10.17987/icfj.v16i0.569","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.569","url":null,"abstract":"We present an interesting case of a middle-aged male patient with recent diagnosis of diffuse large B-cell lymphoma, who underwent a staging CT scan that revealed hypoattenuated lesions in the right atrium initially suspicious of thrombi. They were not evidence on transthoracic echocardiography, but the transesophageal echocardiogram showed a large mobile mass infiltrating and extending the right atrium, interatrial septum and aortic root. This case further illustrates the excellent sensitivity and specificity of transesophageal echocardiography for intracardiac masses but also the importance of multimodality cardiac imaging to reach a diagnosis and guide management. ","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"93 7 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87663302","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}
Background: Hypothermia is well known to elevate the time constant (whatever model is used) of the isochoric left-ventricular pressure fall. Due to different critera in use, it remained unclear whether prolonged diastole in hypothermia is sufficient for complete relaxation. Detecting and quantifying incomplete relaxation may become a valuable tool to prevent diastolic heart failure in hypothermia.Methods: Left-ventricular pressure decays in isolated guinea pig and rat hearts are analysed by 4-parametric regression at different temperatures, at sinus rhythm and electrical stimulation. Residual contraction (F_RC) is introduced and quantified by extrapolating the model's pressure forecast to end-systole, subtracting the asymptote, and normalising.Resultts: Isochoric pressure decay fits the regression model at all temperatures and heart beat frequencies. Residual contraction is virtually absent at normothermia and remains very small (F_RC<3%) down to 31°C. Lower temperatures or pacing induces higher F_RC. Eventually, the pressure curve becomes considerably elevated and looses its concavity.Conclusions: Despite slower pressure fall, ventricular relaxation remains fairly complete at hypothermia; and depends on considerable autoregulation of the individual heart. It is concluded (not proved) that individual emergence of negative lusitropy may indicate imminent heart failure. Asymptotic pressure rises are interpreted at higher ventricular tonus, independent from velocity of relaxation. Gradual increasing time constants may be attributed to a general slowing of bioreactions as temperature falls. Remarkable curve shape changes may be caused by aftercontractions due to elevated Ca++ sensitivity at hypothermia and high Ca++ load by pacing.
{"title":"Left-Ventricular Pressure Relaxation and Diastolic Function of Isolated Working Mammalian Hearts at Hypothermia","authors":"S. F. Langer","doi":"10.17987/icfj.v16i0.538","DOIUrl":"https://doi.org/10.17987/icfj.v16i0.538","url":null,"abstract":"Background: Hypothermia is well known to elevate the time constant (whatever model is used) of the isochoric left-ventricular pressure fall. Due to different critera in use, it remained unclear whether prolonged diastole in hypothermia is sufficient for complete relaxation. Detecting and quantifying incomplete relaxation may become a valuable tool to prevent diastolic heart failure in hypothermia.Methods: Left-ventricular pressure decays in isolated guinea pig and rat hearts are analysed by 4-parametric regression at different temperatures, at sinus rhythm and electrical stimulation. Residual contraction (F_RC) is introduced and quantified by extrapolating the model's pressure forecast to end-systole, subtracting the asymptote, and normalising.Resultts: Isochoric pressure decay fits the regression model at all temperatures and heart beat frequencies. Residual contraction is virtually absent at normothermia and remains very small (F_RC<3%) down to 31°C. Lower temperatures or pacing induces higher F_RC. Eventually, the pressure curve becomes considerably elevated and looses its concavity.Conclusions: Despite slower pressure fall, ventricular relaxation remains fairly complete at hypothermia; and depends on considerable autoregulation of the individual heart. It is concluded (not proved) that individual emergence of negative lusitropy may indicate imminent heart failure. Asymptotic pressure rises are interpreted at higher ventricular tonus, independent from velocity of relaxation. Gradual increasing time constants may be attributed to a general slowing of bioreactions as temperature falls. Remarkable curve shape changes may be caused by aftercontractions due to elevated Ca++ sensitivity at hypothermia and high Ca++ load by pacing.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"73 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2019-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90585854","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}
Abstract:Kara Newport, the CEO of Filoli, describes the instrumental role the landscape plays at this historic house and garden in Woodside, California. After describing the history of Filoli's garden, Newport outlines the process in which staff maintains the garden's integrity while also addressing new landscape use and retaining historic viewsheds. Critical to this story is the role of climate change and other modern challenges such as the availability of water.
{"title":"Adapting to Maintain a Timeless Garden at Filoli","authors":"Kara Newport","doi":"10.1353/FMJ.2018.0020","DOIUrl":"https://doi.org/10.1353/FMJ.2018.0020","url":null,"abstract":"Abstract:Kara Newport, the CEO of Filoli, describes the instrumental role the landscape plays at this historic house and garden in Woodside, California. After describing the history of Filoli's garden, Newport outlines the process in which staff maintains the garden's integrity while also addressing new landscape use and retaining historic viewsheds. Critical to this story is the role of climate change and other modern challenges such as the availability of water.","PeriodicalId":32119,"journal":{"name":"International Cardiovascular Forum Journal","volume":"45 1","pages":"61 - 69"},"PeriodicalIF":0.0,"publicationDate":"2019-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86670935","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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