2013 Vol. 10, No. 1
Background Implantable cardioverter-defibrillator (ICD) leads might not be extracted especially in developing countries because of the high cost and lack of specialized tools. We aimed to evaluate transvenous extraction of ICD leads using optimized standard techniques. Methods We prospectively analyzed clinical characteristics, optimized extraction techniques and the feasibility of extraction for 40 patients (33 males; mean age 47.9 ? 16.1 years) with 42 ICD leads. Results Complete procedural success rate was 95.2% (40/42), and the clinical success rate was 97.6% (41/42). One ICD lead required cardiothoracic surgery. Minor complications occurred in three cases (7.5%), and no major complications or death occurred. Locking stylets were used to extract most leads (34, 81.0%) and almost half of the leads (20, 47.6%) required mechanical dilatation to free fibrotic adhesions; these leads had been implanted for a longer period of time than the others (43.7 ± 18.2 vs. 18.4 ± 13.4 months, P r = 0.70, P Conclusions Our optimized procedure for transvenous extraction of ICD leads provides a practical and low-cost method for standard procedures.
Background The prognosis of elderly patients with chronic total occlusion (CTO) and diabetes mellitus (DM) treated with percutaneous coronary intervention (PCI) is not known. Objective To investigate the effect of diabetes on long-term follow-up of CTO after PCI in elderly patients. Methods A total of 153 elderly patients (age > 65 years old) with CTO lesions which were successfully treated with PCI were enrolled. Fifty one patients with diabetes and 102 without diabetes were compared for long-term outcomes (mean follow up: 36 ? 12 months). Major adverse cardiac events (MACE) which include death, myocardial infarction or target lesion revascularization (TLR) were considered as a combined endpoint. Results The combined endpoint occurred in 29.4% of diabetes patients, and 11.3% of the patients without diabetes (P P = 0.004), DM (HR: 6.69, 95% CI: 1.62–15.81, P = 0.01) and final minimal lumen diameter (MLD) (HR: 0.37, 95% CI: 0.13–0.90, P = 0.03 ) as independent predictors of MACE, DM with renal impairment (HR: 6.64, 95% CI: 1.32–33.36, P = 0.02), HBA1C on admission (HR: 1.79, 95% CI: 1.09–2.94, P = 0.02), as independent predictors of MACE at long term follow-up. Conclusions The study demonstrates that DM is a predictive factor for MACE in elderly CTO patients treated with PCI, type of stent, final minimal lumen diameter and DM with renal impairment, and HBA1C level on admission are predictors of MACE.
Objective Coronary artery ectasia (CAE) refers to abnormal dilation of coronary artery segments to 1.5 times of adjacent normal ones. Epicardial fat is associated with cardiovascular risk factors. The relationship between CAE and epicardial fat has not yet been investigated. This study aimed to assess the relationship between CAE and epicardial fat volume (EFV) in older people by dual-source computed tomography coronary angiography (CTCA). Methods We prospectively enrolled 1400 older adults who were scheduled for dual-source CTCA. Under reconstruction protocols, patients with abnormal segments 1.5 times larger than the adjacent segments were accepted as CAE. EFV was measured by semi-automated software. Traditional risk factors in CAE patients, as well as the extent of EFV, were analyzed and compared to non-CAE group. Results A total of 885 male and 515 female older patients were enrolled. CAE was identified by univariable analysis in 131 patients and significantly correlated to hypertension, smoking, hyperlipidemia, prior percutaneous coronary intervention and ascending aorta aneurysm. EFV was shown to be significantly higher in CAE patients than patients without ectasia. In multivariable analyses, EFV (P = 0.018), hypertension (P P Conclusions CAE can be reliably recognized by dual-source CTCA. Epicardial fat might play a role in etiopathogenesis and progression of CAE, providing a new target for treating ectasia.
Objective To assess the prevalence of and related risk factors for aspirin resistance in elderly patients with coronary artery disease (CAD). Methods Two hundred and forty-six elderly patients (75.9 ± 7.4 years) with CAD who received daily aspirin therapy (≥ 75 mg) over one month were recruited. The effect of aspirin was assessed using light transmission aggregometry (LTA) and thrombelastography platelet mapping assay (TEG). Aspirin resistance was defined as ≥ 20% arachidonic acid (AA)-induced aggregation and ≥ 70% adenosine diphosphate (ADP)-induced aggregation in the LTA assay. An aspirin semi-responder was defined as meeting one (but not both) of the criteria described above. Based on the results of TEG, aspirin resistance was defined as ≥ 50% aggregation induced by AA. Results As determined by LTA, 23 (9.3%) of the elderly CAD patients were resistant to aspirin therapy; 91 (37.0%) were semi-responders. As determined by TEG, 61 patients (24.8%) were aspirin resistant. Of the 61 patients who were aspirin resistant by TEG, 19 were aspirin resistant according to LTA results. Twenty-four of 91 semi-responders by LTA were aspirin resistant by TEG. Multivariate logistic regression analysis revealed that elevated fasting serum glucose level (Odds ratio: 1.517; 95% CI: 1.176–1.957; P = 0.001) was a significant risk factor for aspirin resistance as determined by TEG. Conclusions A significant number of elderly patients with CAD are resistant to aspirin therapy. Fasting blood glucose level is closely associated with aspirin resistance in elderly CAD patients.
Objective To examine the relationship between sex hormone–binding globulin (SHBG) and the metabolic syndrome (MetS) in pre-elderly and elderly men in China. Methods A cross-sectional study was done among 437 men, aged 45 to 94 years old. Early morning fasting sera were assayed for total testosterone (TT), SHBG and other biochemical markers. Free testosterone (FT) was calculated. Results The SHBG level of the MetS group was significantly lower than those without MetS 35.70 (25.18, 47.10) nmol/L vs. 41.90 (31.80, 55.20) nmol/L; P P = 0.018) and homeostasis model assessment for insulin resistance (HOMA-IR) (95%CI: 1.535-2.647, P Conclusions Lower SHBG is independently associated with MetS among pre-elderly and elderly men. SHBG may be an independent predictor of MetS, but the mechanism of how SHBG is involved in MetS requires further studied.
Objective To study whether miR-214 is regulated in coronary artery disease (CAD) patients and whether placental growth factor (PLGF) is a possible target for miR-214 in atherosclerosis. Methods Circulating miR-214 was measured by quantitative PCR using RNA isolated from 40 patients with CAD, including 12 with stable angina pectoris, 16 with unstable angina pectoris and 12 with acute myocardial infarction, and 15 controls without CAD. Plasma level of PLGF was measured by ELISA. Results The miR-214 level was significantly lower in CAD patients compared with that in controls (P P = 0.012, UAP vs. Control; P = 0.005, AMI vs. Control). In patients with AMI, the plasma level of miR-214 was positively correlated to that of PLGF. Conclusions The results suggest that miR-214 is a beneficial microRNA for CAD patients. Loss of its protection may lead to increased PLGF levels and worsening atherosclerosis. Circulating miR-214 is a promising biomarker for alerting severe CAD.
Objective To investigate the effect of nerve growth factor (NGF) on the action potential and potassium currents of non-infarcted myocardium in the myocardial infarcted rabbit model. Methods Rabbits with occlusion of the left anterior descending coronary artery were prepared and allowed to recover for eight weeks (healed myocardial infarction, HMI). During ligation surgery of the left coronary artery, a polyethylene tube was placed near the left stellate ganglion in the subcutis of the neck for the purpose of administering NGF 400 U/d for eight weeks (HMI + NGF group). Cardiomyocytes were isolated from regions of the non-infarcted left ventricular wall and the action potentials and ion currents in these cells were recorded using whole-cell patch clamps. Results Compared with HMI and control cardiomyocytes, significant prolongation of APD50 or APD90 (Action potential duration (APD) measured at 50% and 90% of repolarization) in HMI + NGF cardiomyocytes was found. The results showed that the 4-aminopyridine sensitive transient outward potassium current (Ito), the rapidly activated omponent of delayed rectifier potassium current (IKr), the slowly activated component of delayed rectifier potassium current (IKs), and the L-type calcium current (ICaL) were significantly altered in NGF + HMI cardiomyocytes compared with HMI and control cells. Conclusions Our results suggest that NGF treatment significantly prolongs APD in HMI cardiomyocytes and that a decrease in outward potassium currents and an increase of inward Ca2+ current are likely the underlying mechanism of action.
Objective To investigate the effects of tirofiban on the no-reflow phenomenon of acute myocardial infarction (AMI) rats received reperfusion, as well as the underlying mechanisms. Methods Fifty-six male Sprague-Dawley rats were randomly divided into four groups: Sham operation group (Sham), AMI/reperfusion group (AMI/R), Tirofiban group (Tiro) and Tiro+N-nitro-L-arginine group (L-NNA; an endothelial nitric oxide synthase inhibitor). To generate the animal model mimicking the no-reflow phenomenon, the rats first received occlusion of the left anterior descending coronary artery for 60 min and then followed by reperfusion for 120 min. Area of no-reflow, area at risk and area of necrosis were measured by thioflavine S, Evans blue and triphenyl tetrazolium chloride staining, respectively. Haemodynamic function was measured at the end. In the meantime, nitric oxide synthase (NOS) activity was determined by a NOS assay kit. The expression of myocardial endothelial nitric oxide synthase (eNOS) was determined by an enzyme-linked immunosorbent assay (ELISA). The expression of phosphorylated eNOS at ser sup>1177 (p-eNOS ser1177) and vascular endothelial-cadherin (VE-cadherin) were determined by western blot. Results Compared with AMI/R group, tirofiban significantly reduced the no-reflow area and infarct size (all P 1177 phosphorylated eNOS and VE-cadherin in the ischemic myocardium (all P P Conclusions Tirofiban could reduce the size of no-reflow and infarct. A possible mechanism underlying this effect is that tirofiban could protect the structural and functional integrity of microvascular endothelium which is partially regulated by eNOS activity.
Background Angiotensinogen (AGT) T174M gene polymorphism has been suggested to be linked to risk of coronary artery disease, however, results from studies of this association have been inconsistent. In this study, we assess the relationship between AGT T174M gene polymorphism and coronary artery disease. Methods We conducted a meta-analysis of 18 case-control studies with 8,147 coronary artery disease cases and 5,344 controls in Google scholar, PubMed, Cochrane Library and China National Knowledge Infrastructure (CNKI) databases to identify eligible studies published by July, 2012. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated from these studies. Results Overall, a significant association was found between angiotensinogen T174M polymorphism and coronary artery disease risk when all studies were pooled into the meta-analysis (TT vs. MM: OR = 0.53, 95% CI = 0.40–0.71; dominant model: OR = 1.16, 95% CI = 1.01–1.35; recessive model: OR = 0.54, 95% CI = 0.40–0.72). In a stratified analysis, the results indicate a significant associa?tion in Caucasians suffering from coronary stenosis (TT vs. MM: OR = 0.38, 95% CI = 0.23–0.63; recessive model: OR = 0.39, 95% CI = 0.23–0.64). No significant increased risk for coronary artery disease was found in Asians. Conclusions The meta-analysis indicate a significant associa?tion of T174M polymorphism with coronary stenosis risk in Caucasians.
It is estimated that the elderly (> 65 years of age) will increase from 13%?14% to 25% by 2035. If this trend continues, > 50% of the United States population and more than two billion people worldwide will be “aged” in the next 50 years. Aged individuals face formidable challenges to their health, as aging is associated with a myriad of diseases. Cardiovascular disease is the leading cause of morbidity and mortality in the United States with > 50% of mortality attributed to coronary artery disease and > 80% of these deaths occurring in those age 65 and older. Therefore, age is an important predictor of cardiovascular disease. The efficiency of youth is built upon cellular signaling scaffolds that provide tight and coordinated signaling. Lipid rafts are one such scaffold of which caveolae are a subset. In this review, we consider the importance of caveolae in common cardiovascular diseases of the aged and as potential therapeutic targets. We specifically address the role of caveolin in heart failure, myocardial ischemia, and pulmonary hypertension.
Brugada syndrome is an inherited disease associated with an increased risk of lethal ventricular arrhythmias. Such arrhythmias stem from innate disruptions in cardiac electrophysiology. Typically, such arrhythmias occur in the third or fourth decade of life. However, Brugada syndrome may also affect geriatric patients. In this paper, we focus on the ageing patient with Brugada syndrome, and specifically, on the interaction between Brugada syndrome and the more usually acquired clinical problems that may occur with increasing age, such as the use of cardiovascular and non-cardiovascular drugs, or the need for surgery. Such common conditions may also disrupt cardiac electrophysiology, thereby conferring added risk for Brugada syndrome patients. We present some considerations and recommendations that may serve as guidance to address these complexities.
Percutaneous coronary intervention is a mainstay in the management of symptomatic or high-risk coronary artery disease. The bulk of clinical evidence and experience underlying this fact relies, however, on relatively young patients. Indeed, few data of very limited quality are available which adequately define the risk-benefit and cost-benefit profile of coronary angioplasty and stenting in very old subjects, such as those of 90 years of age or older (i.e., nonagenarians). The aim of this review is to provide a concise, yet practical, synthesis of the available evidence on percutaneous coronary revascularization in the very elderly. The main arguments elaborated upon are to what extent we can extrapolate findings from studies including younger patients to nonagenarians, whether we should provide higher priority to prognosis or quality of life in such patients, and whether we can afford to allocate vast resources to care for such subjects in an era of financial constraints. Our review of 18 studies and 1082 patients suggest that percutaneous coronary intervention is feasible and associated with acceptable short- and long-term results in this population, which is nonetheless fraught with a high mortality risk irrespective of the revascularization procedure. Accordingly, the pros and cons of percutaneous coronary intervention should be carefully weighed when considering this treatment in nonagenarians.
Genetic investigations of cardiomyopathy in the recent two decades have revealed a large number of mutations in the genes encoding sarcomeric proteins as a cause of inherited hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), or restrictive cardiomyopathy (RCM). Most functional analyses of the effects of mutations on cardiac muscle contraction have revealed significant changes in the Ca2+-regulatory mechanism, in which cardiac troponin (cTn) plays important structural and functional roles as a key regulatory protein. Over a hundred mutations have been identified in all three subunits of cTn, i.e., cardiac troponins T, I, and C. Recent studies on cTn mutations have provided plenty of evidence that HCM- and RCM-linked mutations increase cardiac myofilament Ca2+ sensitivity, while DCM-linked mutations decrease it. This review focuses on the functional consequences of mutations found in cTn in terms of cardiac myofilament Ca2+ sensitivity, ATPase activity, force generation, and cardiac troponin I phosphorylation, to understand potential molecular and cellular pathogenic mechanisms of the three types of inherited cardiomyopathy.
Cardiac troponin is the preferred biomarker for the diagnosis of acute myocardial infarction (AMI). The recent development of a high-sensitive cardiac troponin T (hs-cTnT) assay permits detection of very low levels of cTnT. Using the hs-cTnT assay improves the overall diagnostic accuracy in patients with suspected AMI, while a negative result also has a high negative predictive value. The gain in sensitivity may be particularly important in patients with a short duration from symptom onset to admission. Measurement of cardiac troponin T with the hs-cTnT assay may provide strong prognostic information in patients with acute coronary syndromes, stable coronary artery disease, heart failure and even in the general population; however, increased sensitivity comes at a cost of decreased specificity. Serial testing, as well as clinical context and co-existing diseases, are likely to become increasingly important for the interpretation of hs-cTnT assay results.
Coronary aneurysms represent anomalies identified in 0.15%–4.9% of patients undergoing coronary angiography. At present, there is no uniform definition of this pathology. Aneurysms of the left main coronary artery (LMCA) are extremely uncommon, with an incidence of 0.1%. It has been demonstrated that atherosclerosis is the main cause of these anomalies in adults, and Kawasaki disease in children and adolescents. Other causes include connective tissue disorders, trauma, vasculitis, congenital, mycotic, and idiopathic. These dilated sections of the coronary artery are not benign pathology because they are subject to spasm, thrombosis, and subsequent distal embolism, spontaneous dissection and rupture. Treatment options include anticoagulation, custom-made covered stents, reconstruction, resection, and exclusion with bypass. Our report on an old case illustrates the giant saccular LMCA aneurysm leading to myocardial ischemia due to coronary steal phenomenon.
Rivastigmine transdermal patch is indicated for patients with Alzheimer’s disease and dementia with Parkinson’s disease. Rivastigmine, an acetylcholinesterase inhibitor, has several common adverse effects, mainly involving the gastrointestinal tract, but few cardiovascular adverse effects have been reported. This report presents two cases of patients presenting with 3rd degree atrioventricular block. Both patients were treated with the acetylcholinesterase inhibitor, rivastigmine. In one case, the patient reverted to normal sinus rhythm following the discontinuation of rivastigmine, and the atrioventricular block reappeared after rivastigmine was reinstated. In the other case, the atrioventricular block did not revert and the patient required a permanent pacemaker. Both bradycardia and syncope have previously been reported as adverse events in patients treated with acetylcholinesterase inhibitors. However, the type of bradycardia and the etiology of the syncope are rarely specified. Rivastigmine, and other acetylcholinesterase inhibitors, are widely used in the pharmacological treatment of Alzheimer′s disease. We recommend that physicians are vigilant of possible warning signs, such as dizziness, syncope and bradycardia.
Carotid body tumors (CBT) are rare chemical receptor tumors. We report nine cases of CBT who were diagnosed at our center during 2004 to 2008 with a literature review. Of these nine patients, eight underwent complete resection, one received palliative resection due to the malignant nature of the tumor, and the other one refused surgery. No perioperative mortality and stroke occurred. During a mean follow up of 2.2 years, no deaths related to CBT occurred. Surgical treatment for CBT is relatively safe. The surgeon should be careful to maintain the integrity of carotid artery, and prevent cerebral ischemia and cranial nerve injuries in order to improve outcome.