Pub Date : 2017-01-01DOI: 10.35841/CARDIOLOGY.1.1.19-20
W. Qureshi, T. Nguyen, M. Al-Mallah
A 73-year old African-American woman with history of hypertension, diabetes mellitus, liver cirrhosis, atrial fibrillation and diastolic heart failure presented with a one-week history of shortness of breath, increasing dyspnea, eight-pound weight gain, and progressive weakness. She had associated orthopnea, paroxysmal nocturnal dyspnea, and leg swelling. She denied fevers, cough, chills, hemoptysis, recent hospitalization or wheezing. Her initial vitals were: blood pressure 194/127 mmHg, heart rate 74 beats per minute (bpm), respiratory rate 22 and she was afebrile. Examination revealed elevated jugular venous pressure 15 cm above sternal notch at 45 degrees, loud P2, right ventricular heave but regular rate and rhythm. There was a holosystolic murmur grade II/VI present at the left lower sternal border consistent with regurgitation murmur, which increased with inspiration. Initial electrocardiogram showed sinus rhythm with occasional premature ventricular complexes with predominant rightward axis and echocardiogram demonstrated elevated right ventricular systolic pressure of 102 mmHg indicative of severe pulmonary hypertension. The left ventricular ejection fraction was preserved.
{"title":"Individualizing heart failure core measures and use of beta blockers insevere pulmonary hypertension?a teachable moment","authors":"W. Qureshi, T. Nguyen, M. Al-Mallah","doi":"10.35841/CARDIOLOGY.1.1.19-20","DOIUrl":"https://doi.org/10.35841/CARDIOLOGY.1.1.19-20","url":null,"abstract":"A 73-year old African-American woman with history of hypertension, diabetes mellitus, liver cirrhosis, atrial fibrillation and diastolic heart failure presented with a one-week history of shortness of breath, increasing dyspnea, eight-pound weight gain, and progressive weakness. She had associated orthopnea, paroxysmal nocturnal dyspnea, and leg swelling. She denied fevers, cough, chills, hemoptysis, recent hospitalization or wheezing. Her initial vitals were: blood pressure 194/127 mmHg, heart rate 74 beats per minute (bpm), respiratory rate 22 and she was afebrile. Examination revealed elevated jugular venous pressure 15 cm above sternal notch at 45 degrees, loud P2, right ventricular heave but regular rate and rhythm. There was a holosystolic murmur grade II/VI present at the left lower sternal border consistent with regurgitation murmur, which increased with inspiration. Initial electrocardiogram showed sinus rhythm with occasional premature ventricular complexes with predominant rightward axis and echocardiogram demonstrated elevated right ventricular systolic pressure of 102 mmHg indicative of severe pulmonary hypertension. The left ventricular ejection fraction was preserved.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"29 1","pages":"19-20"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87280260","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 : 2017-01-01DOI: 10.35841/CARDIOLOGY.1.1.5-7
Ramyashree Tummala, Sushruth Edla, Jayanthi Ch, rashekaran, K. Ravakhah, AnjanGupta
Brugada Syndrome (BrS) is an autosomal dominant genetic disease determined by abnormal electrocardiographic (ECG) pattern and causes increased risk of sudden cardiac death. It is characterised by coved-type ST segment elevation in precordial leads V1-V3. There had been many proposed mechanisms explaining the link of sodium channel mutations and its electrophysiology. There are various triggering factors like fever, hypokalemia, ischemia, cocaine abuse and medications which unmask the ECG changes and these changes are usually transient. There is increased possibility of this cardiac rhythm to deteriorate into life threatening arrhythmias. Thus it is essential for the clinician to be aware of the conditions. We present such a scenario in which hyperthermia unmasked our patient’s Brugada syndrome.
{"title":"Fever induced Brugada syndrome masquerading as STEMI","authors":"Ramyashree Tummala, Sushruth Edla, Jayanthi Ch, rashekaran, K. Ravakhah, AnjanGupta","doi":"10.35841/CARDIOLOGY.1.1.5-7","DOIUrl":"https://doi.org/10.35841/CARDIOLOGY.1.1.5-7","url":null,"abstract":"Brugada Syndrome (BrS) is an autosomal dominant genetic disease determined by abnormal electrocardiographic (ECG) pattern and causes increased risk of sudden cardiac death. It is characterised by coved-type ST segment elevation in precordial leads V1-V3. There had been many proposed mechanisms explaining the link of sodium channel mutations and its electrophysiology. There are various triggering factors like fever, hypokalemia, ischemia, cocaine abuse and medications which unmask the ECG changes and these changes are usually transient. There is increased possibility of this cardiac rhythm to deteriorate into life threatening arrhythmias. Thus it is essential for the clinician to be aware of the conditions. We present such a scenario in which hyperthermia unmasked our patient’s Brugada syndrome.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"134 1","pages":"5-7"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77390672","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 : 2017-01-01DOI: 10.35841/cardiology.1.1.3-4
Landi Su, Maura Knapp, Rongxue Wu
Aryl hydrocarbon receptor nuclear translocator (ARNT), also known as hypoxia-inducible factor-1 beta (HIF-1β), is a transcription factor that functions as a master regulator of glucose homeostasis. We have previously demonstrated that ARNT expression is highest in the heart, where it is required for maintaining normal cardiac metabolism and cardiac function. Diabetes is associated with a loss of ARNT, although the specific role of ARNT in the diabetic heart is still unknown. Diabetes is also characterized by endothelial dysfunction. Thus, investigating the role of endothelial ARNT in diabetic cardiovascular disease could lead to new therapies for treatment or prevention.
{"title":"Possible role for HIF-1?/ARNT in the regulation of vascular function in diabetes and cardiovascular disease","authors":"Landi Su, Maura Knapp, Rongxue Wu","doi":"10.35841/cardiology.1.1.3-4","DOIUrl":"https://doi.org/10.35841/cardiology.1.1.3-4","url":null,"abstract":"Aryl hydrocarbon receptor nuclear translocator (ARNT), also known as hypoxia-inducible factor-1 beta (HIF-1β), is a transcription factor that functions as a master regulator of glucose homeostasis. We have previously demonstrated that ARNT expression is highest in the heart, where it is required for maintaining normal cardiac metabolism and cardiac function. Diabetes is associated with a loss of ARNT, although the specific role of ARNT in the diabetic heart is still unknown. Diabetes is also characterized by endothelial dysfunction. Thus, investigating the role of endothelial ARNT in diabetic cardiovascular disease could lead to new therapies for treatment or prevention.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"9 1","pages":"3-4"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88926289","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 : 2017-01-01DOI: 10.35841/CARDIOLOGY.1.2.33-38
R. Wagle, M. Cheitlin
From the ancient Greek Olympics to the high school gymnasium, competitive sports have become an increasingly important part of human culture. At an early age, children around the world are introduced and encouraged into sports by their parents and peers. For some, playing sports becomes a regular part of life even as they enter adulthood. The medical profession has always been encouraging of physical activity. With the rising obesity epidemic, even the recent Obama administration, spearheaded by First Lady Michelle Obama, started a campaign called “Let’s Move” to promote exercise among our children. Regular physical activity has been shown to improve many markers of health and can ward off diseases fraught with high morbidity and mortality, like diabetes and obesity. However, as the intensity level of sports increases, there remains controversy as to the advantages of certain vigorous forms of exercise. In rare but dramatic circumstances, young athletes can experience sudden cardiac death on the playing field. There are some evidence-based guidelines to help the cardiologist manage the young athlete before they step foot onto the playing field, but major differences exist in different countries as to how this evidence is interpreted and how cost-effectiveness plays a role.
{"title":"Sudden death on the playing field: Can we prevent it?","authors":"R. Wagle, M. Cheitlin","doi":"10.35841/CARDIOLOGY.1.2.33-38","DOIUrl":"https://doi.org/10.35841/CARDIOLOGY.1.2.33-38","url":null,"abstract":"From the ancient Greek Olympics to the high school gymnasium, competitive sports have become an increasingly important part of human culture. At an early age, children around the world are introduced and encouraged into sports by their parents and peers. For some, playing sports becomes a regular part of life even as they enter adulthood. The medical profession has always been encouraging of physical activity. With the rising obesity epidemic, even the recent Obama administration, spearheaded by First Lady Michelle Obama, started a campaign called “Let’s Move” to promote exercise among our children. Regular physical activity has been shown to improve many markers of health and can ward off diseases fraught with high morbidity and mortality, like diabetes and obesity. However, as the intensity level of sports increases, there remains controversy as to the advantages of certain vigorous forms of exercise. In rare but dramatic circumstances, young athletes can experience sudden cardiac death on the playing field. There are some evidence-based guidelines to help the cardiologist manage the young athlete before they step foot onto the playing field, but major differences exist in different countries as to how this evidence is interpreted and how cost-effectiveness plays a role.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"35 1","pages":"33-38"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79713186","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 : 2017-01-01DOI: 10.35841/cardiology.1.1.1-2
Fan Wang
Coronary artery disease (CAD) and its major complication myocardial infarction (MI) are the leading causes of death worldwide, which often occurs with the accumulation of atherosclerotic plaques in the walls of the coronary arteries. The heritability of CAD has been estimated between 40% and 60%, indicating genetic factor holds an equal or more important contribution to risk of CAD with the other traditional risk factors (i.e., lipid abnormalities, smoking, hypertension, diabetes, and obesity) [1]. In the genetics studies of CAD, the primary goal is to identify causative variants, genes or genetic loci that contribute to the risk of CAD. Given the fact that many risk factors are also strongly are modulated by genetic factors, Mendelian Randomization studies have been designed to estimate causative effects of risk factors on CAD, singlenucleotide polymorphisms (SNPs) servers as instruments [2]. Due to the clinical heterogeneity of CAD, the genetic architecture of CAD is not fully elucidated yet.
{"title":"Genetics of coronary artery disease","authors":"Fan Wang","doi":"10.35841/cardiology.1.1.1-2","DOIUrl":"https://doi.org/10.35841/cardiology.1.1.1-2","url":null,"abstract":"Coronary artery disease (CAD) and its major complication myocardial infarction (MI) are the leading causes of death worldwide, which often occurs with the accumulation of atherosclerotic plaques in the walls of the coronary arteries. The heritability of CAD has been estimated between 40% and 60%, indicating genetic factor holds an equal or more important contribution to risk of CAD with the other traditional risk factors (i.e., lipid abnormalities, smoking, hypertension, diabetes, and obesity) [1]. In the genetics studies of CAD, the primary goal is to identify causative variants, genes or genetic loci that contribute to the risk of CAD. Given the fact that many risk factors are also strongly are modulated by genetic factors, Mendelian Randomization studies have been designed to estimate causative effects of risk factors on CAD, singlenucleotide polymorphisms (SNPs) servers as instruments [2]. Due to the clinical heterogeneity of CAD, the genetic architecture of CAD is not fully elucidated yet.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73856878","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 : 2017-01-01DOI: 10.35841/CARDIOLOGY.1.1.15-18
Ashraf Alqaqa
Atrial fibrillation stands as one of the most common supraventricular arrhythmias. Its incidence in general population has escalated significantly over the last few decades. The health-related quality of life (HRQoL) of patients with atrial fibrillation is currently a vital concern in cardiovascular health management. Accordingly, key elements of meager HRQoL of AF patients demand better clarification. Nowadays, several reports have tested the mutual relation between anxiety and AF initiation and progression. Significantly, anxiety affects how the patients approach their disease and, additionally, anxiety may affect the efficiency of various AF therapies. The goal of this research is to explore an area that considered by patients to be challenging before the therapeutic work-up. Study concluded that there is a multifaceted relationship between AF and anxiety. AF can ground anxiety among patients and equally, anxiety can pave a background that is favorable for the initiation and Progression of AF.
{"title":"Anxiety and atrial fibrillation: an interesting bidirectional association.","authors":"Ashraf Alqaqa","doi":"10.35841/CARDIOLOGY.1.1.15-18","DOIUrl":"https://doi.org/10.35841/CARDIOLOGY.1.1.15-18","url":null,"abstract":"Atrial fibrillation stands as one of the most common supraventricular arrhythmias. Its incidence in general population has escalated significantly over the last few decades. The health-related quality of life (HRQoL) of patients with atrial fibrillation is currently a vital concern in cardiovascular health management. Accordingly, key elements of meager HRQoL of AF patients demand better clarification. Nowadays, several reports have tested the mutual relation between anxiety and AF initiation and progression. Significantly, anxiety affects how the patients approach their disease and, additionally, anxiety may affect the efficiency of various AF therapies. The goal of this research is to explore an area that considered by patients to be challenging before the therapeutic work-up. Study concluded that there is a multifaceted relationship between AF and anxiety. AF can ground anxiety among patients and equally, anxiety can pave a background that is favorable for the initiation and Progression of AF.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"98 1","pages":"15-18"},"PeriodicalIF":0.0,"publicationDate":"2017-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80934699","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}
M. Zaman, R. Gorantla, H. Uppal, N. Lavu, R. Potluri
Cardiac protection is a broad term that refers to all strategies aimed at the attenuation of the damage caused by myocardial ischaemia (MI) and reperfusion. The term is used both in the experimental and clinical field, embracing a very wide (too wide in fact!) range of conditions from reduction of coronary atherosclerosis progression to an immediate reduction of the myocardial infarct size due to acute ischaemia and/or reperfusion. There is no doubt that cardiac protection is a story of broad success but there are also some failures. Indeed, the progression of coronary atherosclerosis can be reduced with angiotensin II inhibitors and statins with a consequential improvement of outcome. Equally, after the demonstration that coronary thrombosis is the cause and not the result of MI, timely restoration of blood flow (reperfusion) has become the standard treatment for these patients, with a corresponding limitation of infarct size, long-term improvement of MI and, more importantly, a reduction in mortality. Despite this success, however, the process of late restoration of blood flow to the ischaemic myocardium can paradoxically induce injury, a phenomenon known as reperfusion injury (RI). Therefore, the major challenge of cardiac protection today is to reduce RI. The problem is that RI is a complex phenomenon, involving many unclearly defined players, all contributing to the final damage that is inflicted on the heart. RI was originally described as a cell swelling, hyper-contracture or disruption of the intra-cellular structure and, in time, has progressed to at least four other types of cardiac dysfunction such as: myocardial stunning, the no-reflow phenomenon, reperfusion arrhythmias and finally lethal reperfusion injury described as an independent mediator of cardiomyocyte death (either necrosis, apoptosis, autophagy or necroptosis), different from ischaemic injury. Several approaches to reduce RI were tried with antioxidants, aderosine, beta and CA2+ blockers, statins, glucose with or without insulin and K, Trimetazidine, cyclosporine and other inhibitors of the Ca2+ pore – all without success. Recently, non-pharmacological interventions have also been proposed to reduce RI, mainly pre and post conditioning. The ideas come from the experimental laboratory, showing that brief cycles of ischaemia and reperfusion performed before a prolonged coronary occlusion or after reperfusion reduced infarct size in dogs. However, when applied to the clinic (mainly post-conditioning as pre-conditioning is difficult) protocols produced good results in small, proof of concept trials but not in a large randomised clinical trial.
{"title":"Angioplasty improves mortality in the managment of acute coronary syndrome in patients with chronic anaemia","authors":"M. Zaman, R. Gorantla, H. Uppal, N. Lavu, R. Potluri","doi":"10.1159/000442375","DOIUrl":"https://doi.org/10.1159/000442375","url":null,"abstract":"Cardiac protection is a broad term that refers to all strategies aimed at the attenuation of the damage caused by myocardial ischaemia (MI) and reperfusion. The term is used both in the experimental and clinical field, embracing a very wide (too wide in fact!) range of conditions from reduction of coronary atherosclerosis progression to an immediate reduction of the myocardial infarct size due to acute ischaemia and/or reperfusion. There is no doubt that cardiac protection is a story of broad success but there are also some failures. Indeed, the progression of coronary atherosclerosis can be reduced with angiotensin II inhibitors and statins with a consequential improvement of outcome. Equally, after the demonstration that coronary thrombosis is the cause and not the result of MI, timely restoration of blood flow (reperfusion) has become the standard treatment for these patients, with a corresponding limitation of infarct size, long-term improvement of MI and, more importantly, a reduction in mortality. Despite this success, however, the process of late restoration of blood flow to the ischaemic myocardium can paradoxically induce injury, a phenomenon known as reperfusion injury (RI). Therefore, the major challenge of cardiac protection today is to reduce RI. The problem is that RI is a complex phenomenon, involving many unclearly defined players, all contributing to the final damage that is inflicted on the heart. RI was originally described as a cell swelling, hyper-contracture or disruption of the intra-cellular structure and, in time, has progressed to at least four other types of cardiac dysfunction such as: myocardial stunning, the no-reflow phenomenon, reperfusion arrhythmias and finally lethal reperfusion injury described as an independent mediator of cardiomyocyte death (either necrosis, apoptosis, autophagy or necroptosis), different from ischaemic injury. Several approaches to reduce RI were tried with antioxidants, aderosine, beta and CA2+ blockers, statins, glucose with or without insulin and K, Trimetazidine, cyclosporine and other inhibitors of the Ca2+ pore – all without success. Recently, non-pharmacological interventions have also been proposed to reduce RI, mainly pre and post conditioning. The ideas come from the experimental laboratory, showing that brief cycles of ischaemia and reperfusion performed before a prolonged coronary occlusion or after reperfusion reduced infarct size in dogs. However, when applied to the clinic (mainly post-conditioning as pre-conditioning is difficult) protocols produced good results in small, proof of concept trials but not in a large randomised clinical trial.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2015-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83586280","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}
R. Nunes, V. Giampaoli, H. Freitas, A. Pereira, F. Araujo, G. Correia, M. Rondon, C. Negrão, A. Mansur, G. Charach, A. Rabinovich, Argov Ori, D. Weksler, D. Sheps, L. Charach, M. Weintraub, J. George, M. Link, Fatemeh Khorashadizadeh, M. Ghayour-Mobarhan, G. Ferns, A. Budzikowski, P. Akhrass, K. Li, Tao Zhang, H. Fan, Qinchuan Li, Wulf Ito, J. Torzewski, J. Guo, Zhongmin Liu, Jie Liu, Shuxia Wang, Jinxin Shi, Yuanyuan Guo, Jianfeng Liu, Tao Tao, Ping Zhu, V. Serebruany, D. Sibbing, J. DiNicolantonio, A. Levine, Lionel Levine, T. Levine, C. Knutson, Ali Erayman, T. Kawada, A. Rahsepar, Faisal Latif, Lijun Tian, Jun Zhu, Lisheng Liu, Yan Liang, Jiandong Li, Yanmin Yang, Ş. Balta, M. Demir, S. Demırkol, U. Kucuk, M. Unlu, Z. Arslan, U. Thadani, Satz Mengensatzproduktion, Druckerei Stückle
{"title":"Front and Back Matter","authors":"R. Nunes, V. Giampaoli, H. Freitas, A. Pereira, F. Araujo, G. Correia, M. Rondon, C. Negrão, A. Mansur, G. Charach, A. Rabinovich, Argov Ori, D. Weksler, D. Sheps, L. Charach, M. Weintraub, J. George, M. Link, Fatemeh Khorashadizadeh, M. Ghayour-Mobarhan, G. Ferns, A. Budzikowski, P. Akhrass, K. Li, Tao Zhang, H. Fan, Qinchuan Li, Wulf Ito, J. Torzewski, J. Guo, Zhongmin Liu, Jie Liu, Shuxia Wang, Jinxin Shi, Yuanyuan Guo, Jianfeng Liu, Tao Tao, Ping Zhu, V. Serebruany, D. Sibbing, J. DiNicolantonio, A. Levine, Lionel Levine, T. Levine, C. Knutson, Ali Erayman, T. Kawada, A. Rahsepar, Faisal Latif, Lijun Tian, Jun Zhu, Lisheng Liu, Yan Liang, Jiandong Li, Yanmin Yang, Ş. Balta, M. Demir, S. Demırkol, U. Kucuk, M. Unlu, Z. Arslan, U. Thadani, Satz Mengensatzproduktion, Druckerei Stückle","doi":"10.1159/000357886","DOIUrl":"https://doi.org/10.1159/000357886","url":null,"abstract":"","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"17 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2013-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85332558","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 : 2011-03-01DOI: 10.3923/TCARD.2011.20.24
R. M. Silva, Livio Bruno Santos Cunha, Loyara Rocha Miranda Teixeira, M. A. Dias
{"title":"Correlation of P-wave Duration and Dispersion in Patients with Ischemia-Induced During Treadmill Exercise Testing with Duke Score","authors":"R. M. Silva, Livio Bruno Santos Cunha, Loyara Rocha Miranda Teixeira, M. A. Dias","doi":"10.3923/TCARD.2011.20.24","DOIUrl":"https://doi.org/10.3923/TCARD.2011.20.24","url":null,"abstract":"","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"19 1","pages":"20-24"},"PeriodicalIF":0.0,"publicationDate":"2011-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75156193","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}
S. Chakravarthi, H. Nagaraja, C. Wei, Wong Shew Fung, M. J. Wah, A. Radhakrishnan
Candidiasis is a fungal infection which patients with solid malignancies are at high risk. While few studies have shown evidence of this disease co-existing with malignancy-induced immunosuppression disease, there never were any exclusive animal studies demonstrating this relationship, especially cardiac candidiasis with breast cancer. In fact, the exact causative mechanism of candidiasis is by and large still under much speculation. This study aims to demonstrate this relationship by observing the histopathological changes of the hearts harvested from female Balb/c mice which were experimentally induced with breast cancer and inoculated with Candida. The mice were randomly assigned to 5 different groups (n = 12). The first group (group 1) was injected with Phosphate Buffer Solution (PBS), the second group (group 2) with Candida, third group (Group 3) with breast cancer and the final two groups, fourth and fifth group (Group 4 and 5) having co-existence of candidiasis and breast cancer at 2 different doses of candidiasis, respectively. Inoculation of mice with candidiasis was done by intravenous injection of Candida albicans via the tail vein after successful culturing methods. Induction of mice with breast cancer is via injection of 4T1 cancer cells at the right axillary mammary fatpad after effective culturing methods. The prepared slides with the livers were stained with Haematoxylin and Eos in (H and E), Periodic Acidic Schiff (PAS) and Gomori Methenamine Silver (GMS) stains for histopathology analysis. Grading of primary tumour and identification of metastatic deposits were done. Scoring of inflammation and congestion in the liver was done. Statistical tests done to compare group 2 and 4 showed that group 4 exhibited a highly statistically significant increase in inflammation and congestion (p<0.01). The median severity of candidiasis was also increased in group 4 as compared to group 2. In conclusion, based on the above evidences, cardiac candidiasis was significantly increased in mice with breast cancer.
念珠菌病是一种真菌性感染，合并实体恶性肿瘤的患者患病风险较高。虽然很少有研究表明这种疾病与恶性诱导的免疫抑制疾病共存，但从未有任何专门的动物研究证明这种关系，特别是心脏念珠菌病与乳腺癌。事实上，念珠菌病的确切致病机制在很大程度上仍处于许多猜测之中。本研究旨在通过观察Balb/c雌性小鼠实验诱导乳腺癌并接种念珠菌的心脏组织病理学变化来证明这种关系。将小鼠随机分为5组(n = 12)。第一组(1组)注射磷酸缓冲液(PBS)，第二组(2组)注射念珠菌，第三组(3组)注射乳腺癌，最后两组，第四组和第五组(4组和5组)分别注射2种不同剂量的念珠菌病，念珠菌病与乳腺癌共存。培养方法成功后，通过尾静脉静脉注射白色念珠菌接种念珠菌病小鼠。通过有效的培养方法，在右侧腋窝乳腺脂肪垫注射4T1癌细胞诱导小鼠乳腺癌。用血红素和Eos in (H和E)，周期性酸性希夫(PAS)和Gomori甲基胺银(GMS)染色进行组织病理学分析。对原发肿瘤进行分级，并对转移灶进行鉴定。对肝脏炎症和充血进行评分。比较第2组和第4组的统计学检验显示，第4组的炎症和充血增加具有高度统计学意义(p<0.01)。与第2组相比，第4组念珠菌病的中位严重程度也有所增加。综上所述，乳腺癌小鼠心脏念珠菌感染明显增加。
{"title":"A histopathological study of cardiac candidiasis and its behaviour under immunosuppressive effect of disseminated breast carcinoma","authors":"S. Chakravarthi, H. Nagaraja, C. Wei, Wong Shew Fung, M. J. Wah, A. Radhakrishnan","doi":"10.3923/TCARD.2011.1.7","DOIUrl":"https://doi.org/10.3923/TCARD.2011.1.7","url":null,"abstract":"Candidiasis is a fungal infection which patients with solid malignancies are at high risk. While few studies have shown evidence of this disease co-existing with malignancy-induced immunosuppression disease, there never were any exclusive animal studies demonstrating this relationship, especially cardiac candidiasis with breast cancer. In fact, the exact causative mechanism of candidiasis is by and large still under much speculation. This study aims to demonstrate this relationship by observing the histopathological changes of the hearts harvested from female Balb/c mice which were experimentally induced with breast cancer and inoculated with Candida. The mice were randomly assigned to 5 different groups (n = 12). The first group (group 1) was injected with Phosphate Buffer Solution (PBS), the second group (group 2) with Candida, third group (Group 3) with breast cancer and the final two groups, fourth and fifth group (Group 4 and 5) having co-existence of candidiasis and breast cancer at 2 different doses of candidiasis, respectively. Inoculation of mice with candidiasis was done by intravenous injection of Candida albicans via the tail vein after successful culturing methods. Induction of mice with breast cancer is via injection of 4T1 cancer cells at the right axillary mammary fatpad after effective culturing methods. The prepared slides with the livers were stained with Haematoxylin and Eos in (H and E), Periodic Acidic Schiff (PAS) and Gomori Methenamine Silver (GMS) stains for histopathology analysis. Grading of primary tumour and identification of metastatic deposits were done. Scoring of inflammation and congestion in the liver was done. Statistical tests done to compare group 2 and 4 showed that group 4 exhibited a highly statistically significant increase in inflammation and congestion (p<0.01). The median severity of candidiasis was also increased in group 4 as compared to group 2. In conclusion, based on the above evidences, cardiac candidiasis was significantly increased in mice with breast cancer.","PeriodicalId":22442,"journal":{"name":"The Cardiology","volume":"57 1","pages":"1-7"},"PeriodicalIF":0.0,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76898880","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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