2009 Vol. 6, No. 1
Display Method:
2009, 6(1): 3-10.
Abstract:
Background and Objective Diastolic dysfunction of the left ventricle is a mechanical abnormality diagnosed primarily by echocardiogram, and can be distinguished into three separate degrees based on the severity of reduction in passive compliance and active myocardial relaxation. Methods A literature search was performed for basic science studies, clinical studies and major practice guidelines on the subject of diastolic dysfunction and diastolic heart failure. Important findings were analyzed and correlated with regard to clinical relevance. Results Left ventricular diastolic dysfunction appears to compromise exercise tolerance and is believed to contribute to the pathophysiology in patients with diastolic heart failure. In the clinical setting, however, oftentimes no clear distinction is made between echocardiographically diagnosed diastolic dysfunction and diastolic heart failure, and adequate treatment recommendations are sparse and aimed to prevent worsening and progression of clinical symptoms. To date, there is a lack of high powered trials assessing the possible progression rate from echocardiographically diagnosed diastolic dysfunction to the clinical diagnosis of diastolic heart failure. Furthermore, there are no solid indices to assess the degree of severity of diastolic dysfunction or its progression. Pure right ventricular diastolic dysfunction appears to be even less understood and under-recognized, although it may play a role in the development of both right and left heart failure. Currently there are few but interesting data on the possible interaction between ventricles with diastolic dysfunction and the overall affect on the development of heart failure. Conclusions The timeline and progression of diastolic dysfunction to diastolic heart failure have not been well established and warrant further investigation.
Background and Objective Diastolic dysfunction of the left ventricle is a mechanical abnormality diagnosed primarily by echocardiogram, and can be distinguished into three separate degrees based on the severity of reduction in passive compliance and active myocardial relaxation. Methods A literature search was performed for basic science studies, clinical studies and major practice guidelines on the subject of diastolic dysfunction and diastolic heart failure. Important findings were analyzed and correlated with regard to clinical relevance. Results Left ventricular diastolic dysfunction appears to compromise exercise tolerance and is believed to contribute to the pathophysiology in patients with diastolic heart failure. In the clinical setting, however, oftentimes no clear distinction is made between echocardiographically diagnosed diastolic dysfunction and diastolic heart failure, and adequate treatment recommendations are sparse and aimed to prevent worsening and progression of clinical symptoms. To date, there is a lack of high powered trials assessing the possible progression rate from echocardiographically diagnosed diastolic dysfunction to the clinical diagnosis of diastolic heart failure. Furthermore, there are no solid indices to assess the degree of severity of diastolic dysfunction or its progression. Pure right ventricular diastolic dysfunction appears to be even less understood and under-recognized, although it may play a role in the development of both right and left heart failure. Currently there are few but interesting data on the possible interaction between ventricles with diastolic dysfunction and the overall affect on the development of heart failure. Conclusions The timeline and progression of diastolic dysfunction to diastolic heart failure have not been well established and warrant further investigation.
2009, 6(1): 11-19.
Abstract:
Protein S deficiency is an autosomal dominant disorder that results from mutations in the protein S gene (PROS1). Inherited deficiency of protein S constitutes a risk factor for venous thromboembolism. Protein S functions as a nonenzymatic cofactor for activated protein C in the proteolytic degradation of coagulation factors Ⅴa and Ⅷa. The frequency of protein S deficiency seems to differ between populations. More than 200 rare mutations in PROS1 have been identified in patients with protein S deficiency. Among the prevalent mutations within PROS1, the S460P substitution (known as Heerlen polymorphism) detected in Caucasians and the K196E substitution (known as protein S Tokushima) found in Japanese have been intensively studied for their structures and potential functions in the disorder of protein S deficiency. Until now, causative mutations in PROS1 have been found in only approximately 50% of cases with protein S deficiency. Co-segregation analysis of microsatellite haplotypes with protein S deficiency in families with protein S deficiency suggests that the causative defects in the PROS1 mutation-negative patients are located in or close to the PROS1 gene. Large PROS1 gene deletions have been identified in 3 out of 9 PROS1 mutation-negative Swedish VTE families with protein S deficiency and 1 out of 6 PROS1 mutation-negative Japanese patients with protein S deficiency. Intensive sequencing of the entire PROS1 gene, including introns, may be needed to identify the cryptic mutations in those patients, and these efforts might uncover the pathogenesis of protein S deficiency.
Protein S deficiency is an autosomal dominant disorder that results from mutations in the protein S gene (PROS1). Inherited deficiency of protein S constitutes a risk factor for venous thromboembolism. Protein S functions as a nonenzymatic cofactor for activated protein C in the proteolytic degradation of coagulation factors Ⅴa and Ⅷa. The frequency of protein S deficiency seems to differ between populations. More than 200 rare mutations in PROS1 have been identified in patients with protein S deficiency. Among the prevalent mutations within PROS1, the S460P substitution (known as Heerlen polymorphism) detected in Caucasians and the K196E substitution (known as protein S Tokushima) found in Japanese have been intensively studied for their structures and potential functions in the disorder of protein S deficiency. Until now, causative mutations in PROS1 have been found in only approximately 50% of cases with protein S deficiency. Co-segregation analysis of microsatellite haplotypes with protein S deficiency in families with protein S deficiency suggests that the causative defects in the PROS1 mutation-negative patients are located in or close to the PROS1 gene. Large PROS1 gene deletions have been identified in 3 out of 9 PROS1 mutation-negative Swedish VTE families with protein S deficiency and 1 out of 6 PROS1 mutation-negative Japanese patients with protein S deficiency. Intensive sequencing of the entire PROS1 gene, including introns, may be needed to identify the cryptic mutations in those patients, and these efforts might uncover the pathogenesis of protein S deficiency.
2009, 6(1): 20-25.
Abstract:
Background Evaluation of acute myocardial infarction after reperfusion by dual phase contrast-enhancement multislice computed tomography (MSCT) was implicated in porcine model. There have been few attempts to use this diagnostic modality for the early assessment of coronary reperfusion in patients with ST-elevation myocardial infarction (STEMI), especially after primary percutaneous coronary intervention (PCI). In elderly patients with STEMI, the safety issues remain unknown. Methods Dual phase contrast-enhancement MSCT examinations were performed in 11 elderly patients (≥60 years old ) with STEMI within one week after primary PCI. The presence, location and enhancement pattern on MSCT were evaluated. MSCT findings were compared with the catheter angiographic results and area under the curve of creatine kinase (CK) release. Serum creatinine level was recorded before and after MSCT scan. Results MSCT scans were successfully performed in all the patients. Early myocardial perfusion defect (early defect, ED) was detected in all of the 11 patients (100%) in the early phase of the contrast bolus (subendocardial ED in 10 patients and transmural in 1 patient). Mean CT attenuation value of ED was significantly different from CT attenuation value of remote myocardium (46 ± 17 HU vs 104 ± 17 HU; P < 0.01). Location of ED area correlated well with infarction related artery territory on catheter angiography in all of the 11 patients (100%). On delayed phase of MSCT scan, different enhancement patterns were observed: isolated subendocardial late enhancement (LE) in 6 patients, subendocardial residual perfusion defect (RD) and subepicardial LE in 1 patient, subendocardial RD in 4 patients. Infarct volume assessed by MSCT correlated well with area under the curve CK release (R=0.72, P <0.01). Serum creatinine level after MSCT scan showed no difference with that before MSCT scan. Conclusion Dual phase MSCT could be safely implicated in elderly patients with STEMI. Variable abnormal myocardial enhancement patterns were seen on dual phase MSCT in these patients with STEMI after primary PCI. Assessment of myocardial attenuation on MSCT gives additional information of the location and extent of infarction after reperfusion.
Background Evaluation of acute myocardial infarction after reperfusion by dual phase contrast-enhancement multislice computed tomography (MSCT) was implicated in porcine model. There have been few attempts to use this diagnostic modality for the early assessment of coronary reperfusion in patients with ST-elevation myocardial infarction (STEMI), especially after primary percutaneous coronary intervention (PCI). In elderly patients with STEMI, the safety issues remain unknown. Methods Dual phase contrast-enhancement MSCT examinations were performed in 11 elderly patients (≥60 years old ) with STEMI within one week after primary PCI. The presence, location and enhancement pattern on MSCT were evaluated. MSCT findings were compared with the catheter angiographic results and area under the curve of creatine kinase (CK) release. Serum creatinine level was recorded before and after MSCT scan. Results MSCT scans were successfully performed in all the patients. Early myocardial perfusion defect (early defect, ED) was detected in all of the 11 patients (100%) in the early phase of the contrast bolus (subendocardial ED in 10 patients and transmural in 1 patient). Mean CT attenuation value of ED was significantly different from CT attenuation value of remote myocardium (46 ± 17 HU vs 104 ± 17 HU; P < 0.01). Location of ED area correlated well with infarction related artery territory on catheter angiography in all of the 11 patients (100%). On delayed phase of MSCT scan, different enhancement patterns were observed: isolated subendocardial late enhancement (LE) in 6 patients, subendocardial residual perfusion defect (RD) and subepicardial LE in 1 patient, subendocardial RD in 4 patients. Infarct volume assessed by MSCT correlated well with area under the curve CK release (R=0.72, P <0.01). Serum creatinine level after MSCT scan showed no difference with that before MSCT scan. Conclusion Dual phase MSCT could be safely implicated in elderly patients with STEMI. Variable abnormal myocardial enhancement patterns were seen on dual phase MSCT in these patients with STEMI after primary PCI. Assessment of myocardial attenuation on MSCT gives additional information of the location and extent of infarction after reperfusion.
2009, 6(1): 26-30.
Abstract:
Objective Accelerated left main coronary stenosis (LMCS) is a known potential late complication of coronary artery catheter procedures. The aim of this study was to assess the current occurrence of LMCS as a delayed complication of percutaneous angioplasty (PTCA) of the left coronary branches in our institution. Methods The medical records of patients referred for coronary artery by-pass surgery from the same Cardiology Unit in the January 2003 to December 2006 period and presenting a significant (>50%) LMCS as a new finding following a PTCA of the left coronary artery branches, were reviewed. Patients with retrospective evidence of any LMCS at previous coronary angiographies preceding the percutaneous procedure were excluded. Results Thirty-seven patients (5 females, mean age 71.1±8.6 years) out of 944 (4%) having undergone a PTCA, fulfilled the inclusion criteria, 19 (51%) after a procedure also involving the LAD coronary artery. Extraback-up guiding catheters were used in most cases. Use of multiple wires or balloons was observed in 3 cases (8%). Rotablator and proximal occlusion device were used in one case respectively (3%). Twenty patients (54%) have had more than one percutaneous coronary intervention on the left coronary branches. The mean time elapsed from the first angioplasty and surgical intervention was 18.1±7.8 months. Conclusions The potential occurrence of LMCS following a percutaneous intervention procedure, especially when complicated and repeated, should not be underestimated in the current era. This evidence may offer the rationale to schedule non-invasive imaging tests to monitor left main coronary patency after the procedure as well as to fuel further research to develop less traumatic materials.
Objective Accelerated left main coronary stenosis (LMCS) is a known potential late complication of coronary artery catheter procedures. The aim of this study was to assess the current occurrence of LMCS as a delayed complication of percutaneous angioplasty (PTCA) of the left coronary branches in our institution. Methods The medical records of patients referred for coronary artery by-pass surgery from the same Cardiology Unit in the January 2003 to December 2006 period and presenting a significant (>50%) LMCS as a new finding following a PTCA of the left coronary artery branches, were reviewed. Patients with retrospective evidence of any LMCS at previous coronary angiographies preceding the percutaneous procedure were excluded. Results Thirty-seven patients (5 females, mean age 71.1±8.6 years) out of 944 (4%) having undergone a PTCA, fulfilled the inclusion criteria, 19 (51%) after a procedure also involving the LAD coronary artery. Extraback-up guiding catheters were used in most cases. Use of multiple wires or balloons was observed in 3 cases (8%). Rotablator and proximal occlusion device were used in one case respectively (3%). Twenty patients (54%) have had more than one percutaneous coronary intervention on the left coronary branches. The mean time elapsed from the first angioplasty and surgical intervention was 18.1±7.8 months. Conclusions The potential occurrence of LMCS following a percutaneous intervention procedure, especially when complicated and repeated, should not be underestimated in the current era. This evidence may offer the rationale to schedule non-invasive imaging tests to monitor left main coronary patency after the procedure as well as to fuel further research to develop less traumatic materials.
2009, 6(1): 31-37.
Abstract:
Background and Objective The frequency of multifocal atherosclerosis (MFA) in patients with coronary heart disease (CHD) has not been thoroughly studied. The purpose of our study was to perform ultrasound screening for MFA in patients with coronary atherosclerosis and make evaluation of the sensitivity and significance of different atherosclerosis markers. Methods Using Color Dupplex Ultrasound (CDU), we studied 32 clinically healthy persons and 87 patients of the city of B with clinical data for CHD where we also performed coronarography. Results In patients with coronary atherosclerosis we found high frequency of carotid atherosclerosis (93%) and peripheral artery disease (PAD) (81%). We established verifiable thickening of the intima-media (IMT) of the common carotid artery (CCA) and common femoral artery (CFA) in patients with CHD. There is a correlation between the frequency of carotid and femoral stenoses and CHD proven by coronarography. Patients with CHD had a high relative risk to develop carotid (RR = 5) and peripheral atherosclerosis (RR = 3.5) and high frequency of asymptomatic stenoses and thromboses of the internal carotid artery (86.9%) and femoral artery (78.3%), as well as aneurisms of the abdominal aorta (8.1%). Markers for CAD with high sensitivity were the atherosclerotic plaques of ICA (0.93) and CFA (0.81) as well as IMT of the CFA (0.84). Conclusions MFA are common among patients with CHD. Ultrasound diagnosis is the method of choice for simultaneous non-invasive screening of carotid, peripheral and MFA and provides sensitive markers for coronary atherosclerosis. The most sensitive and specific markers for CHD are the combination of the IMT and atherosclerotic plaques of CCA, ICA and CFA (100% sensitivity and 0.92 specificity).
Background and Objective The frequency of multifocal atherosclerosis (MFA) in patients with coronary heart disease (CHD) has not been thoroughly studied. The purpose of our study was to perform ultrasound screening for MFA in patients with coronary atherosclerosis and make evaluation of the sensitivity and significance of different atherosclerosis markers. Methods Using Color Dupplex Ultrasound (CDU), we studied 32 clinically healthy persons and 87 patients of the city of B with clinical data for CHD where we also performed coronarography. Results In patients with coronary atherosclerosis we found high frequency of carotid atherosclerosis (93%) and peripheral artery disease (PAD) (81%). We established verifiable thickening of the intima-media (IMT) of the common carotid artery (CCA) and common femoral artery (CFA) in patients with CHD. There is a correlation between the frequency of carotid and femoral stenoses and CHD proven by coronarography. Patients with CHD had a high relative risk to develop carotid (RR = 5) and peripheral atherosclerosis (RR = 3.5) and high frequency of asymptomatic stenoses and thromboses of the internal carotid artery (86.9%) and femoral artery (78.3%), as well as aneurisms of the abdominal aorta (8.1%). Markers for CAD with high sensitivity were the atherosclerotic plaques of ICA (0.93) and CFA (0.81) as well as IMT of the CFA (0.84). Conclusions MFA are common among patients with CHD. Ultrasound diagnosis is the method of choice for simultaneous non-invasive screening of carotid, peripheral and MFA and provides sensitive markers for coronary atherosclerosis. The most sensitive and specific markers for CHD are the combination of the IMT and atherosclerotic plaques of CCA, ICA and CFA (100% sensitivity and 0.92 specificity).
2009, 6(1): 38-41.
Abstract:
Objective To investigate the relationship of blood pressure circadian rhythm with myocardial hypertrophy and the changes of autonomic nerve function in patients with essential hypertension (EH). Methods Eighty-two female patients with essential hypertension (EH) underwent 24-hours ambulatory blood pressure monitorings (ABPM), dynamic electrocardiogram (Holter) and echocardiography examination. Patients were classified into non-dipping group (n=40) and dipping group (n=42) according to the result of ABPM. Left ventricular mass index (LVMI), heart rate variability (HRV) in time domain (including SDNN, SDANN, rMSSD, PNN50) and heart rate turbulence (HRT) parameters (including turbulence onset [TO] and turbulence slope [TS]) were measured. Results Compared with those in dipping group, patients in non-dipping group have higher incidence of LVH (19.0% vs 52.5%, P<0.01), greater mean LVMI (112.39±12.79 g/m2 vs 121.98±13.35 g/m2, P<0.01), decreased PNN50 and rMSSD. TS value was decreased while TO was increased in non-dipping group compared with those in dipping group (both P <0.01); patients with LVH showed decreased TS and increased TO, compared with those without LVH. Conclusion In female patients with EH, non-dipping blood pressure circadian is associated with higher incidence of LVH. The HRV and HRT were more remarkably blunted in non-dipping patients, as well as those with LVH.
Objective To investigate the relationship of blood pressure circadian rhythm with myocardial hypertrophy and the changes of autonomic nerve function in patients with essential hypertension (EH). Methods Eighty-two female patients with essential hypertension (EH) underwent 24-hours ambulatory blood pressure monitorings (ABPM), dynamic electrocardiogram (Holter) and echocardiography examination. Patients were classified into non-dipping group (n=40) and dipping group (n=42) according to the result of ABPM. Left ventricular mass index (LVMI), heart rate variability (HRV) in time domain (including SDNN, SDANN, rMSSD, PNN50) and heart rate turbulence (HRT) parameters (including turbulence onset [TO] and turbulence slope [TS]) were measured. Results Compared with those in dipping group, patients in non-dipping group have higher incidence of LVH (19.0% vs 52.5%, P<0.01), greater mean LVMI (112.39±12.79 g/m2 vs 121.98±13.35 g/m2, P<0.01), decreased PNN50 and rMSSD. TS value was decreased while TO was increased in non-dipping group compared with those in dipping group (both P <0.01); patients with LVH showed decreased TS and increased TO, compared with those without LVH. Conclusion In female patients with EH, non-dipping blood pressure circadian is associated with higher incidence of LVH. The HRV and HRT were more remarkably blunted in non-dipping patients, as well as those with LVH.
2009, 6(1): 42-48.
Abstract:
Objective To explore the role and the possible molecular mechanisms of natural anti-oxLDL IgM monoclonal antibody played and involved in pathogenesis of atherosclerosis. Methods Natural anti-oxLDL IgM monoclonal antibody 3A6 was generated by using standard hybridoma production techniques. Influence of 3A6 on formation of foam cells was observed by Oil Red O staining and affinity of Na125 I-conjugated oxLDL on the na?ve and LPS-activated macrophages. After LPS stimulation on macrophages, anti-TLR4 neutralizing mAb, p38MAPK specific inhibitor SB203580, NF-kB specific inhibitor PDTC or RNAi targeting Fcα/μ receptor (Fcamr) were applied, respectively. Results Natural anti-oxLDL IgM monoclonal antibody 3A6 were found specifically inhibit the binding of CuoxLDL to na?ve macrophages but not the binding of CuoxLDL to LPS-activated macrophages. It also promoted the formation of CuoxLDL-mediated foam macrophages. 3A6 F(ab’)2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. LPS up-regulated the expression of Fcamr in macrophages in a dose- and time-dependent manner, which was attenuated by treatment with anti-TLR4. LPS induced the phosphorylation of p38MAPK and translocation of NF-κB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages. Conclusions Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to na?ve macrophages in vitro. However, LPS, through the Toll-like receptor (TLR)4 receptor, activated the p38MAPK and NF-κB pathways and up-regulated the expression of Fcα/μ receptor in macrophages, which promoted the binding of 3A6/CuoxLDL complex to macrophages through binding with Fc fragments and the formation of foam macrophages. Therefore, our findings provide a new explanation why bacterial infection deteriorates the pathogenesis of atherosclerosis.
Objective To explore the role and the possible molecular mechanisms of natural anti-oxLDL IgM monoclonal antibody played and involved in pathogenesis of atherosclerosis. Methods Natural anti-oxLDL IgM monoclonal antibody 3A6 was generated by using standard hybridoma production techniques. Influence of 3A6 on formation of foam cells was observed by Oil Red O staining and affinity of Na125 I-conjugated oxLDL on the na?ve and LPS-activated macrophages. After LPS stimulation on macrophages, anti-TLR4 neutralizing mAb, p38MAPK specific inhibitor SB203580, NF-kB specific inhibitor PDTC or RNAi targeting Fcα/μ receptor (Fcamr) were applied, respectively. Results Natural anti-oxLDL IgM monoclonal antibody 3A6 were found specifically inhibit the binding of CuoxLDL to na?ve macrophages but not the binding of CuoxLDL to LPS-activated macrophages. It also promoted the formation of CuoxLDL-mediated foam macrophages. 3A6 F(ab’)2 or pre-incubation with un-related IgM inhibited the binding of 3A6/CuoxLDL complex to LPS-activated macrophages. LPS up-regulated the expression of Fcamr in macrophages in a dose- and time-dependent manner, which was attenuated by treatment with anti-TLR4. LPS induced the phosphorylation of p38MAPK and translocation of NF-κB p65, contributing to the up-regulated expression of Fcα/μ receptor in macrophages. Conclusions Natural anti-oxLDL IgM monoclonal antibody 3A6 specifically inhibited the binding of CuoxLDL to na?ve macrophages in vitro. However, LPS, through the Toll-like receptor (TLR)4 receptor, activated the p38MAPK and NF-κB pathways and up-regulated the expression of Fcα/μ receptor in macrophages, which promoted the binding of 3A6/CuoxLDL complex to macrophages through binding with Fc fragments and the formation of foam macrophages. Therefore, our findings provide a new explanation why bacterial infection deteriorates the pathogenesis of atherosclerosis.
2009, 6(1): 49-55.
Abstract:
The endoplasmic reticulum (ER) serves several important functions, mainly post-translational modification, folding and assembly of newly synthesized secretary proteins, synthesizing lipids and cellular calcium storage. Various factors can disrupt ER homeostasis and disturb its functions, which leads to the accumulation of unfolded and misfolded proteins and to potential cellular dysfunction and pathological consequences, collectively termed ER stress. Recent progress suggests that ER stress plays a key role in the immune response, diabetes, tumor growth, and some neurodegenerative diseases. In particular, ER stress is involved in several processes of cardiovascular diseases, such as ischemia/reperfusion injury, cardiomyopathy, cardiac hypertrophy, heart failure, and atherosclerosis. Further research on the relation of ER stress to cardiovascular diseases will greatly enhance the understanding of these pathological processes and provide novel avenues to potential therapies.
The endoplasmic reticulum (ER) serves several important functions, mainly post-translational modification, folding and assembly of newly synthesized secretary proteins, synthesizing lipids and cellular calcium storage. Various factors can disrupt ER homeostasis and disturb its functions, which leads to the accumulation of unfolded and misfolded proteins and to potential cellular dysfunction and pathological consequences, collectively termed ER stress. Recent progress suggests that ER stress plays a key role in the immune response, diabetes, tumor growth, and some neurodegenerative diseases. In particular, ER stress is involved in several processes of cardiovascular diseases, such as ischemia/reperfusion injury, cardiomyopathy, cardiac hypertrophy, heart failure, and atherosclerosis. Further research on the relation of ER stress to cardiovascular diseases will greatly enhance the understanding of these pathological processes and provide novel avenues to potential therapies.
2009, 6(1): 56-61.
Abstract:
Traditional Chinese medicine (TCM) is one of the world’s oldest healing systems. TCM includes herbal medicine, acupuncture, moxibustion, massage, food therapy, and physical exercise, such as shadow boxing. In modern China, TCM is a fully institutionalised part of health care and widely used with Western medicine. In 2006, the TCM sector provided care for over 200 million outpatients and some 7 million inpatients, accounting for 10-20% of health care in China. Numerous studies conducted in China and some in other countries have shown that TCM significantly helps patients with coronary heart disease, hyperlipidemia, hypertension, pericarditis, angina pectoris, tachycardia, atherosclerosis, heart failure, and other circulatory conditions. Many doctors trained with Western medicine now recognize that a combination of Western therapy and TCM has shown better results in improving overall health in patients with cardiovascular disease (CVD) than have modern medicine drugs or surgery alone. In this review, we present a brief outline of TCM for the treatment of CVD, focusing on the two most used TCM therapeutic modalities, Chinese herbal medicine (CHM) and acupuncture. There are huge amounts of Chinese publications on the use of CHM and acupuncture for CVD, but only those published in English will be reviewed here.
Traditional Chinese medicine (TCM) is one of the world’s oldest healing systems. TCM includes herbal medicine, acupuncture, moxibustion, massage, food therapy, and physical exercise, such as shadow boxing. In modern China, TCM is a fully institutionalised part of health care and widely used with Western medicine. In 2006, the TCM sector provided care for over 200 million outpatients and some 7 million inpatients, accounting for 10-20% of health care in China. Numerous studies conducted in China and some in other countries have shown that TCM significantly helps patients with coronary heart disease, hyperlipidemia, hypertension, pericarditis, angina pectoris, tachycardia, atherosclerosis, heart failure, and other circulatory conditions. Many doctors trained with Western medicine now recognize that a combination of Western therapy and TCM has shown better results in improving overall health in patients with cardiovascular disease (CVD) than have modern medicine drugs or surgery alone. In this review, we present a brief outline of TCM for the treatment of CVD, focusing on the two most used TCM therapeutic modalities, Chinese herbal medicine (CHM) and acupuncture. There are huge amounts of Chinese publications on the use of CHM and acupuncture for CVD, but only those published in English will be reviewed here.
2009, 6(1): 62-64.
Abstract:
Aims and Scope: Journal of Geriatric Cardiology (JGC) is a biomedical quarterly published by the Institute of Geriatric Cardiology, China. The purpose of JGC is to provide a forum for the exchange of information, ideas and opinions between physicians and researchers in the east and in the west. JGC publishes peer-reviewed articles that are relevant to the care of older persons with cardiovascular disease, especially those with concomitant disease of other major organ-systems, such as the lungs, the kidneys, liver, central nervous system, gastrointestinal tract or endocrinology, etc. JGC also occasionally republishes, with permission, articles of scientific or clinical excellence that have appeared in Chinese-language journals. Regular features of the Journal include: State-of-the-Art Articles, clinical research, laboratory research, review article, case report, letter to the editor and others.
Aims and Scope: Journal of Geriatric Cardiology (JGC) is a biomedical quarterly published by the Institute of Geriatric Cardiology, China. The purpose of JGC is to provide a forum for the exchange of information, ideas and opinions between physicians and researchers in the east and in the west. JGC publishes peer-reviewed articles that are relevant to the care of older persons with cardiovascular disease, especially those with concomitant disease of other major organ-systems, such as the lungs, the kidneys, liver, central nervous system, gastrointestinal tract or endocrinology, etc. JGC also occasionally republishes, with permission, articles of scientific or clinical excellence that have appeared in Chinese-language journals. Regular features of the Journal include: State-of-the-Art Articles, clinical research, laboratory research, review article, case report, letter to the editor and others.
