2014 Vol. 11, No. 4
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2014, 11(4): 279-285.
doi: 10.11909/j.issn.1671-5411.2014.04.001
Abstract:
Background Evaluation of patient outcomes following transcatheter aortic valve implantation (TAVI) has usually been based on survival and clinical improvement. Studies on quality of life are limited, and data from comprehensive assessments after the procedure are lacking. Methods Sixty patients referred for cardiac rehabilitation after TAVI underwent in-hospital and after-discharge multidimensional assessments to evaluate clinical, functional, and nutritional statuses, degree of autonomy, cognitive impairment, depression and quality of life. Results On admission to rehabilitation, approximately half of the patients had severe functional impairment and dependence for basic activities of daily living. During their hospital stay, one-third of the patients suffered significant clinical complications and two had to be transferred to the implantation center. Despite this, the overall outcome was very good. All of the remaining patients were clinically stable at discharge and functional status, autonomy and quality of life were improved in most. During a mean follow-up of 540 days (range: 192–738 days), five patients died from noncardiac causes, three were hospitalized for cardiac events, and nine for non cardiac reasons. Functional status and autonomy remained satisfactory in the majority of patients and most continued to live independently. Conclusion Patients referred for rehabilitation after TAVI are often very frail, with a high grade of functional impairment, dependence on others and high risk of clinical complications. During a rehabilitation programme, based on a multidimensional assessment and intervention, most patients showed significant improvement in functional status, quality of life, and autonomy, which remained stable in the majority of subjects during mid-term follow-up.
Background Evaluation of patient outcomes following transcatheter aortic valve implantation (TAVI) has usually been based on survival and clinical improvement. Studies on quality of life are limited, and data from comprehensive assessments after the procedure are lacking. Methods Sixty patients referred for cardiac rehabilitation after TAVI underwent in-hospital and after-discharge multidimensional assessments to evaluate clinical, functional, and nutritional statuses, degree of autonomy, cognitive impairment, depression and quality of life. Results On admission to rehabilitation, approximately half of the patients had severe functional impairment and dependence for basic activities of daily living. During their hospital stay, one-third of the patients suffered significant clinical complications and two had to be transferred to the implantation center. Despite this, the overall outcome was very good. All of the remaining patients were clinically stable at discharge and functional status, autonomy and quality of life were improved in most. During a mean follow-up of 540 days (range: 192–738 days), five patients died from noncardiac causes, three were hospitalized for cardiac events, and nine for non cardiac reasons. Functional status and autonomy remained satisfactory in the majority of patients and most continued to live independently. Conclusion Patients referred for rehabilitation after TAVI are often very frail, with a high grade of functional impairment, dependence on others and high risk of clinical complications. During a rehabilitation programme, based on a multidimensional assessment and intervention, most patients showed significant improvement in functional status, quality of life, and autonomy, which remained stable in the majority of subjects during mid-term follow-up.
2014, 11(4): 286-290.
doi: 10.11909/j.issn.1671-5411.2014.04.002
Abstract:
Background QT dispersion (QTd) is a predictor of ventricular arrhythmia. Ventricular arrhythmia is an important factor influencing morbidity and mortality in patients with aortic stenosis. Surgical aortic valve replacement reduced the QTd in this patients group. However, the effect of transcatheter aortic valve implantation (TAVI) on QTd in patients with aortic stenosis is unknown. The aim of this study was to investigate the effect of TAVI on QTd in patients with aortic stenosis. Methods Patients with severe aortic stenosis, who were not candidates for surgical aortic valve replacement due to contraindications or high surgical risk, were included in the study. All patients underwent electrocardiographic and echocardiographic evaluation before, and at the 6th month after TAVI, computed QTd and left ventricular mass index (LVMI). Results A total 30 patients were admitted to the study (mean age 83.2 ± 1.0 years, female 21 and male 9, mean valve area 0.7 ± 3 mm2). Edwards SAPIEN heart valves, 23 mm (21 patients) and 26 mm (9 patients), by the transfemoral approach were used in the TAVI procedures. All TAVI procedures were successful. Both QTd and LVMI at the 6th month after TAVI were significantly reduced compared with baseline values of QTd and LVMI before TAVI (73.8 ± 4 ms vs. 68 ± 2 ms, P = 0.001 and 198 ± 51 g/m2 vs.. 184 ± 40 g/m2, P = 0.04, respectively). There was a significant correlation between QTd and LVMI (r = 0.646, P Conclusion QTd, which malign ventricular arrhythmia marker, and LVMI were significantly reduced after TAVI procedure. TAVI may decrease the possibility of ventricular arrhythmia in patients with aortic stenosis.
Background QT dispersion (QTd) is a predictor of ventricular arrhythmia. Ventricular arrhythmia is an important factor influencing morbidity and mortality in patients with aortic stenosis. Surgical aortic valve replacement reduced the QTd in this patients group. However, the effect of transcatheter aortic valve implantation (TAVI) on QTd in patients with aortic stenosis is unknown. The aim of this study was to investigate the effect of TAVI on QTd in patients with aortic stenosis. Methods Patients with severe aortic stenosis, who were not candidates for surgical aortic valve replacement due to contraindications or high surgical risk, were included in the study. All patients underwent electrocardiographic and echocardiographic evaluation before, and at the 6th month after TAVI, computed QTd and left ventricular mass index (LVMI). Results A total 30 patients were admitted to the study (mean age 83.2 ± 1.0 years, female 21 and male 9, mean valve area 0.7 ± 3 mm2). Edwards SAPIEN heart valves, 23 mm (21 patients) and 26 mm (9 patients), by the transfemoral approach were used in the TAVI procedures. All TAVI procedures were successful. Both QTd and LVMI at the 6th month after TAVI were significantly reduced compared with baseline values of QTd and LVMI before TAVI (73.8 ± 4 ms vs. 68 ± 2 ms, P = 0.001 and 198 ± 51 g/m2 vs.. 184 ± 40 g/m2, P = 0.04, respectively). There was a significant correlation between QTd and LVMI (r = 0.646, P Conclusion QTd, which malign ventricular arrhythmia marker, and LVMI were significantly reduced after TAVI procedure. TAVI may decrease the possibility of ventricular arrhythmia in patients with aortic stenosis.
2014, 11(4): 291-295.
doi: 10.11909/j.issn.1671-5411.2014.04.003
Abstract:
Background Atrial fibrillation (AF) catheter ablation has emerged as a promising treatment strategy for AF, but has not been widely adopted in the elderly population. The present study aimed to determine the safety and efficacy of AF catheter ablation in the elderly population. Methods and Results The study population consisted of 316 patients with paroxysmal AF who underwent left atrial ablation. Ninety-five patients were ≥ 65 years (48 males, mean age 68.9 ± 3.0 years old) and 221 patients were P = 0.169). Procedural complications were uncommon in both study groups. In logistic regression analysis, left atrial diameter (P = 0.003), hypertension (P = 0.001), dyslipidemia (P = 0.039), and coronary artery disease (P = 0.018) were independent predictors of AF recurrence in the elderly population. Conclusion Catheter ablation of AF is safe and effective in older patients. Invasive strategies should be considered as an alternative choice in symptomatic elderly patients with AF.
Background Atrial fibrillation (AF) catheter ablation has emerged as a promising treatment strategy for AF, but has not been widely adopted in the elderly population. The present study aimed to determine the safety and efficacy of AF catheter ablation in the elderly population. Methods and Results The study population consisted of 316 patients with paroxysmal AF who underwent left atrial ablation. Ninety-five patients were ≥ 65 years (48 males, mean age 68.9 ± 3.0 years old) and 221 patients were P = 0.169). Procedural complications were uncommon in both study groups. In logistic regression analysis, left atrial diameter (P = 0.003), hypertension (P = 0.001), dyslipidemia (P = 0.039), and coronary artery disease (P = 0.018) were independent predictors of AF recurrence in the elderly population. Conclusion Catheter ablation of AF is safe and effective in older patients. Invasive strategies should be considered as an alternative choice in symptomatic elderly patients with AF.
2014, 11(4): 296-302.
doi: 10.11909/j.issn.1671-5411.2014.04.004
Abstract:
Background The data on the prognostic values of high sensitivity C-reactive protein (hsCRP) levels in patients with advanced symptomatic heart failure (HF) receiving cardiac resynchronization therapy (CRT) are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP (> 3 mg/L) prior to CRT was associated with a significant 2.39-fold increase (P = 0.006) in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels (–0.5 ± 4.1 mg/L reduction) compared with non-responders (1.7 ± 6.1 mg/L increase, P = 0.018). Compared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations (Log-rank P Conclusion Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.
Background The data on the prognostic values of high sensitivity C-reactive protein (hsCRP) levels in patients with advanced symptomatic heart failure (HF) receiving cardiac resynchronization therapy (CRT) are scarce. The aim of present study was to investigate the association of serum hsCRP levels with left ventricle reverse remodeling after six months of CRT as well as long-term outcome. Methods A total of 232 CRT patients were included. The assessment of hsCRP values, clinical status and echocardiographic data were performed at baseline and after six months of CRT. Long-term follow-up included all-cause mortality and hospitalizations for HF. Results During the mean follow-up periods of 31.3 ± 31.5 months, elevated hsCRP (> 3 mg/L) prior to CRT was associated with a significant 2.39-fold increase (P = 0.006) in the risk of death or HF hospitalizations. At 6-month follow-up, patients who responded to CRT showed significant reductions or maintained low in hsCRP levels (–0.5 ± 4.1 mg/L reduction) compared with non-responders (1.7 ± 6.1 mg/L increase, P = 0.018). Compared with patients in whom 6-month hsCRP levels were reduced or remained low, patients in whom 6-month hsCRP levels were increased or maintained high experienced a significantly higher risk of subsequent death or HF hospitalizations (Log-rank P Conclusion Our findings demonstrated that measurement of baseline and follow-up hsCRP levels may be useful as prognostic markers for timely potential risk stratification and subsequent appropriate treatment strategies in patients with advanced HF undergoing CRT.
2014, 11(4): 303-310.
doi: 10.11909/j.issn.1671-5411.2014.04.005
Abstract:
Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion (I/R) injury and microRNAs (miRNAs) could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pretreatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardioprotection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxygen-glucose deprivation (OGD) on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase (LDH) and creatine kinase (CK) activities, intracellular free Ca2+ concentration ([Ca2+]i) as well as the relative protein levels of sodium/calcium exchanger 1(NCX1), BCL2-like 11 (BIM), calmodulin-dependent protein kinase IIδ (CaMKIIδ) and Cyclophilin D (CypD). Results The in vitro results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining (±dp/dt max). In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR (qPCR) results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Transfection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2+ and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδ and CypD. Conclusion Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.
Background Electroacupuncture pretreatment plays a protective role in myocardial ischemia/reperfusion (I/R) injury and microRNAs (miRNAs) could act on various facets of cardiac function. However, the role of miRNAs in the cardioprotection by electroacupuncture pretreatment on myocardial I/R injury remains unknown. The purpose of the study was to examine whether miR-214 was involved in cardioprotection by electroacupuncture. Methods Using rat myocardial I/R model, we examined the role of electroacupuncture pretreatment in myocardial I/R injury and analyzed the changes in the expression of miR-214. In addition, I/R was simulated in vitro by performing oxygen-glucose deprivation (OGD) on H9c2 cell cultures, and the effect of electroacupuncture pretreatment on I/R injury as well as expressional level of miR-214 were examined in vitro. Furthermore, the miR-214 mimic was transfected into OGD-treated H9c2 cells, we analyzed the cell apoptosis, lactate dehydrogenase (LDH) and creatine kinase (CK) activities, intracellular free Ca2+ concentration ([Ca2+]i) as well as the relative protein levels of sodium/calcium exchanger 1(NCX1), BCL2-like 11 (BIM), calmodulin-dependent protein kinase IIδ (CaMKIIδ) and Cyclophilin D (CypD). Results The in vitro results revealed that compared with the I/R group, the electroacupuncture pretreatment group showed significant decreased myocardial infarct size, as well as the increased indices of the cardiac function, including heart rate, mean arterial pressure, left ventricular systolic pressure and maximal rate for left ventricular pressure rising and declining (±dp/dt max). In addition, electroacupuncture pretreatment could inhibit the elevation of LDH and CK activities induced by I/R injury. The quantitative PCR (qPCR) results demonstrated electroacupuncture pretreatment could provide cardioprotection against myocardial I/R injury in rats with miR-214 up-regulation. In the meanwhile, in vitro, electroacupuncture pretreatment protected H9c2 cells from OGD-induced injury. Transfection of miR-214 mimic showed protective effects on OGD-induced injury to H9c2 cells by reducing apoptosis, decreasing LDH and CK activities, rescuing the OGD-induced Ca2+ and down-regulating elevated protein levels of NCX1, BIM, CaMKIIδ and CypD. Conclusion Our findings firstly demonstrated that electroacupuncture pretreatment promotes the expression of miR-214 in myocardial I/R injury and miR-214 contributes to the protective effect of electroacupuncture on myocardial I/R injury.
2014, 11(4): 311-315.
doi: 10.11909/j.issn.1671-5411.2014.04.006
Abstract:
Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB (NF-κB). The NF-κB transcription factor family includes several subunits (p50, p52, p65, c-Rel, and Rel B) that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Methods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme (AAV9-R65-CMV-eGFP) was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the underlying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65- CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease.
Background Oxidative stress is a major mechanism underlying the pathogenesis of cardiovascular disease. It can trigger inflammatory cascades which are primarily mediated via nuclear factor-κB (NF-κB). The NF-κB transcription factor family includes several subunits (p50, p52, p65, c-Rel, and Rel B) that respond to myocardial ischemia. It has been proved that persistent myocyte NF-κB p65 activation in heart failure exacerbates cardiac remodeling. Methods A recombinant adeno-associated virus serotype 9 carrying enhanced green fluorescent protein and anti-NF-κB p65 ribozyme (AAV9-R65-CMV-eGFP) was constructed. The cells were assessed by MTT assay, Annexin V–propidium iodide dual staining to study apoptosis. The expression of P65 and P50 were assessed by Western blot to investigate the underlying molecular mechanisms. Results After stimulation with H2O2 for 6 h, H9c2 cells viability decreased significantly, a large fraction of cells underwent apoptosis. We observed a rescue of H9c2 cells from H2O2-induced apoptosis in pretreatment with AAV9-R65-CMV-eGFP. Moreover, AAV9-R65-CMV-eGFP decreased H2O2-induced P65 expression. Conclusions AAV9-R65-CMV-eGFP protects H9c2 cells from oxidative stress induced apoptosis through down-regulation of P65 expression. These observations indicate that AAV9-R65- CMV-eGFP has the potential to exert cardioprotective effects against oxidative stress, which might be of great importance to clinical efficacy for cardiovascular disease.
2014, 11(4): 316-328.
doi: 10.11909/j.issn.1671-5411.2014.04.007
Abstract:
Cognitive damage in heart failure (HF) involves different domains thus interfering with the ability for single patient to self-care and to cope with treatment regimens, modifying symptoms and health behaviours. Many cerebral and functional changes were detected in brain imaging, involving areas of both grey and white matter deputed to cognition. Although various instruments are available to explore cognition, no consensus was obtained on better tools to be used in HF population. Reduction in cerebral blood flow, decreased cardiac output, alterations of cerebrovascular reactivity and modification of blood pressure levels are the main features involved in the etiopathogenetic mechanisms of cognitive deficit. Several cardiac variables, laboratory parameters, demographic and clinical elements were studied for their possible relation with cognition and should be properly evaluated to define patients at increased risk of impairment. The present review gathers available data pointing out assured information and discussing possible areas of research development.
Cognitive damage in heart failure (HF) involves different domains thus interfering with the ability for single patient to self-care and to cope with treatment regimens, modifying symptoms and health behaviours. Many cerebral and functional changes were detected in brain imaging, involving areas of both grey and white matter deputed to cognition. Although various instruments are available to explore cognition, no consensus was obtained on better tools to be used in HF population. Reduction in cerebral blood flow, decreased cardiac output, alterations of cerebrovascular reactivity and modification of blood pressure levels are the main features involved in the etiopathogenetic mechanisms of cognitive deficit. Several cardiac variables, laboratory parameters, demographic and clinical elements were studied for their possible relation with cognition and should be properly evaluated to define patients at increased risk of impairment. The present review gathers available data pointing out assured information and discussing possible areas of research development.
2014, 11(4): 329-337.
doi: 10.11909/j.issn.1671-5411.2014.04.008
Abstract:
Chronic heart failure (CHF) is the leading cause of hospitalization for those over the age of 65 and represents a significant clinical and economic burden. About half of hospital re-admissions are related to co-morbidities, polypharmacy and disabilities associated with CHF. Moreover, CHF also has an enormous cost in terms of poor prognosis with an average one year mortality of 33%–35%. While more than half of patients with CHF are over 75 years, most clinical trials have included younger patients with a mean age of 61 years. Inadequate data makes treatment decisions challenging for the providers. Older CHF patients are more often female, have less cardiovascular diseases and associated risk factors, but higher rates of non-cardiovascular conditions and diastolic dysfunction. The prevalence of CHF with reduced ejection fraction, ischemic heart disease, and its risk factors declines with age, whereas the prevalence of non-cardiac co-morbidities, such as chronic renal failure, dementia, anemia and malignancy increases with age. Diabetes and hypertension are among the strongest risk factors as predictors of CHF particularly among women with coronary heart disease. This review paper will focus on the specific consideration for CHF assessment in the older population. Management strategies will be reviewed, including non-pharmacologic, pharmacologic, quality care indicators, quality improvement in care transition and lastly, end-of-life issues. Palliative care should be an integral part of an interdisciplinary team approach for a comprehensive care plan over the whole disease trajectory. In addition, frailty contributes valuable prognostic insight incremental to existing risk models and assists clinicians in defining optimal care pathways for their patients.
Chronic heart failure (CHF) is the leading cause of hospitalization for those over the age of 65 and represents a significant clinical and economic burden. About half of hospital re-admissions are related to co-morbidities, polypharmacy and disabilities associated with CHF. Moreover, CHF also has an enormous cost in terms of poor prognosis with an average one year mortality of 33%–35%. While more than half of patients with CHF are over 75 years, most clinical trials have included younger patients with a mean age of 61 years. Inadequate data makes treatment decisions challenging for the providers. Older CHF patients are more often female, have less cardiovascular diseases and associated risk factors, but higher rates of non-cardiovascular conditions and diastolic dysfunction. The prevalence of CHF with reduced ejection fraction, ischemic heart disease, and its risk factors declines with age, whereas the prevalence of non-cardiac co-morbidities, such as chronic renal failure, dementia, anemia and malignancy increases with age. Diabetes and hypertension are among the strongest risk factors as predictors of CHF particularly among women with coronary heart disease. This review paper will focus on the specific consideration for CHF assessment in the older population. Management strategies will be reviewed, including non-pharmacologic, pharmacologic, quality care indicators, quality improvement in care transition and lastly, end-of-life issues. Palliative care should be an integral part of an interdisciplinary team approach for a comprehensive care plan over the whole disease trajectory. In addition, frailty contributes valuable prognostic insight incremental to existing risk models and assists clinicians in defining optimal care pathways for their patients.
2014, 11(4): 338-348.
doi: 10.11909/j.issn.1671-5411.2014.01.009
Abstract:
A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cytoplasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated catabolic cellular 'housekeeping' process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protective mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the variability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic manipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.
A physiological sequence called autophagy qualitatively determines cellular viability by removing protein aggregates and damaged cytoplasmic constituents, and contributes significantly to the degree of myocardial ischemia-reperfusion (I/R) injury. This tightly orchestrated catabolic cellular 'housekeeping' process provides cells with a new source of energy to adapt to stressful conditions. This process was first described as a pro-survival mechanism, but increasing evidence suggests that it can also lead to the demise of the cell. Autophagy has been implicated in the pathogenesis of multiple cardiac conditions including myocardial I/R injury. However, a debate persists as to whether autophagy acts as a protective mechanism or contributes to the injurious effects of I/R injury in the heart. This controversy may stem from several factors including the variability in the experimental models and species, and the methodology used to assess autophagy. This review provides updated knowledge on the modulation and role of autophagy in isolated cardiac cells subjected to I/R, and the growing interest towards manipulating autophagy to increase the survival of cardiac myocytes under conditions of stress-most notably being I/R injury. Perturbation of this evolutionarily conserved intracellular cleansing autophagy mechanism, by targeted modulation through, among others, mammalian target of rapamycin (mTOR) inhibitors, adenosine monophosphate-activated protein kinase (AMPK) modulators, calcium lowering agents, resveratrol, longevinex, sirtuin activators, the proapoptotic gene Bnip3, IP3 and lysosome inhibitors, may confer resistance to heart cells against I/R induced cell death. Thus, therapeutic manipulation of autophagy in the challenged myocardium may benefit post-infarction cardiac healing and remodeling.
2014, 11(4): 349-353.
doi: 10.11909/j.issn.1671-5411.2014.04.010
Abstract:
Pulmonary thromboembolism (PTE) is a life-threatening condition with a high early mortality rate caused by acute right ventricular failure and cardiogenic shock. We report a series of three patients who presented with acute and subacute submassive PTE. They were successfully treated by simple catheter-based mechanical thrombectomy and intrapulmonary arterial thrombolysis. Mechanical fragmentation and aspiration of thrombus was performed by commonly used J-wire, multi-purpose and Judkin Right guiding catheters and this obviated the need of specific thrombectomy devices.
Pulmonary thromboembolism (PTE) is a life-threatening condition with a high early mortality rate caused by acute right ventricular failure and cardiogenic shock. We report a series of three patients who presented with acute and subacute submassive PTE. They were successfully treated by simple catheter-based mechanical thrombectomy and intrapulmonary arterial thrombolysis. Mechanical fragmentation and aspiration of thrombus was performed by commonly used J-wire, multi-purpose and Judkin Right guiding catheters and this obviated the need of specific thrombectomy devices.
2014, 11(4): 354-356.
doi: 10.11909/j.issn.1671-5411.2014.04.011
Abstract:
Coronary fistulae and ventricular septal perforation are very rare clinically, and even less caused by cardiac leiomyosarcoma. A case is reported that a 67-year-old female had cardiac leiomyosarcoma with progressive heart failure and coronary fistulae and ventricular septal perforation. This case was special since all ante-mortem examinations and cardiac surgery failed to detect the presence of any abnormal cardiac mass. Therefore, the malignant cardiac tumors could appear in an invasive form without mass and be one of the causes of the coronary fistulae and ventricular septal perforation.
Coronary fistulae and ventricular septal perforation are very rare clinically, and even less caused by cardiac leiomyosarcoma. A case is reported that a 67-year-old female had cardiac leiomyosarcoma with progressive heart failure and coronary fistulae and ventricular septal perforation. This case was special since all ante-mortem examinations and cardiac surgery failed to detect the presence of any abnormal cardiac mass. Therefore, the malignant cardiac tumors could appear in an invasive form without mass and be one of the causes of the coronary fistulae and ventricular septal perforation.
2014, 11(4): 357-362.
doi: 10.11909/j.issn.1671-5411.2014.04.012
Abstract:
A 54-year-old female patient with congenital heart disease had a persistent complete left bundle branch block three months after closure by an Amplatzer ventricular septal defect occluder. Nine months later, the patient suffered from chest distress, palpitation, and sweating at daily activities, and her 6-min walk distance decreased significantly (155 m). Her echocardiography showed increased left ventricular end-diastolic diameter with left ventricular ejection fraction of 37%. Her symptoms reduced significantly one week after received cardiac resynchronization therapy. She had no symptoms at daily activities, and her echo showed left ventricular ejection fraction of 46% and 53%. Moreover, left ventricular end-diastolic diameter decreased 6 and 10 months after cardiac resynchronization therapy, and 6-min walk distance remarkably increased. This case demonstrated that persistent complete left bundle branch block for nine months after transcatheter closure with ventricular septal defect Amplatzer occluder could lead to left ventricular enlargement and a significant decrease in left ventricular systolic function. Cardiac resynchronization therapy decreased left ventricular end-diastolic diameter and increased left ventricular ejection fraction, thereby improving the patient’s heart functions.
A 54-year-old female patient with congenital heart disease had a persistent complete left bundle branch block three months after closure by an Amplatzer ventricular septal defect occluder. Nine months later, the patient suffered from chest distress, palpitation, and sweating at daily activities, and her 6-min walk distance decreased significantly (155 m). Her echocardiography showed increased left ventricular end-diastolic diameter with left ventricular ejection fraction of 37%. Her symptoms reduced significantly one week after received cardiac resynchronization therapy. She had no symptoms at daily activities, and her echo showed left ventricular ejection fraction of 46% and 53%. Moreover, left ventricular end-diastolic diameter decreased 6 and 10 months after cardiac resynchronization therapy, and 6-min walk distance remarkably increased. This case demonstrated that persistent complete left bundle branch block for nine months after transcatheter closure with ventricular septal defect Amplatzer occluder could lead to left ventricular enlargement and a significant decrease in left ventricular systolic function. Cardiac resynchronization therapy decreased left ventricular end-diastolic diameter and increased left ventricular ejection fraction, thereby improving the patient’s heart functions.
2014, 11(4): 363-367.
doi: 10.11909/j.issn.1671-5411.2014.04.013
Abstract:
Hemopericardium is a common finding at autopsy, but it may represent a challenge for the forensic pathologist when the etiopathological relationship in causing death is requested. Hemopericardium and cardiac tamponade can be evaluated in living people using radiological techniques, in particular computer tomography (CT). Only a few studies are reported in literature involving post-mortem (PM) cases, where PMCT imaging has been used in order to investigate acute hemopericardium, and they have shown a good accuracy of this technique. Here we report a case involving a 70-year-old white male found dead on the beach, with a medical history of hepatitis C and chronic hypertension with a poor pharmacological response. A PMCT was performed about 3 h after the discovery of the body. The PMCT examination showed an intrapericardial aortic dissection associated to a periaortic hematoma, a sickle-shaped intramural hematoma, a false lumen, and a hemopericardium consisting in fluid and clotted blood. In this case, the PMCT was able to identify the cause of death, even though a traditional autopsy was required to confirm the radiological findings. PMCT is a reliable technique, which in chosen cases, can be performed without the need for a traditional autopsy to be carried out.
Hemopericardium is a common finding at autopsy, but it may represent a challenge for the forensic pathologist when the etiopathological relationship in causing death is requested. Hemopericardium and cardiac tamponade can be evaluated in living people using radiological techniques, in particular computer tomography (CT). Only a few studies are reported in literature involving post-mortem (PM) cases, where PMCT imaging has been used in order to investigate acute hemopericardium, and they have shown a good accuracy of this technique. Here we report a case involving a 70-year-old white male found dead on the beach, with a medical history of hepatitis C and chronic hypertension with a poor pharmacological response. A PMCT was performed about 3 h after the discovery of the body. The PMCT examination showed an intrapericardial aortic dissection associated to a periaortic hematoma, a sickle-shaped intramural hematoma, a false lumen, and a hemopericardium consisting in fluid and clotted blood. In this case, the PMCT was able to identify the cause of death, even though a traditional autopsy was required to confirm the radiological findings. PMCT is a reliable technique, which in chosen cases, can be performed without the need for a traditional autopsy to be carried out.
