2007 Vol. 4, No. 3
Objective To determine anti-cytomegalovirus (CMV) antibodies along with anti-Chlamydia pneumoniae (CP) antibodies in comparison with inflammatory markers and other risk factors of atherosclerosis in patients with selected cardiovascular diseases (CVD). Methods A total of 228 patients with coronary heart disease (CHD) and/or hypertension (HT), and those who underwent reconstructive vascular surgery (RVS) on carotids or abdominal aorta were tested for the presence of anti-CMV IgG and IgM antibodies as well as for anti-CP IgA antibodies, C-reactive protein (CRP), and interleukin-6 (IL-6). Other risk factors for atherosclerosis, namely age, gender, smoking, hypercholesterolemia, and diabetes mellitus were also analyzed. Results Anti-CMV IgG antibodies were found in 204 patients sera (89.5%), compared with 46 positive of 68 sera in the controls (67.6%), whereas anti-CMV IgM antibodies were detected in 4 of 54 sera of patients tested (7.4%), but not in the controls. The highest proportion of positive sera with not only anti-CMV IgG antibodies (95.6.7%), but also anti-CP IgA antibodies (78.3%), IL-6 (84.8%) and CRP (97.8%), was observed in patients with RVS. The results obtained corresponded to age, hypercholesterolemia, and diabetes. Conclusions The presence of anti-CMV antibodies together with antibodies to CP and markers of inflammation (CRP and IL-6) in our study was associated with CVD, primarily in elderly patients who underwent RVS.
It has become clear that inflammation is an important component of coronary heart disease. Atherosclerotic disease usually begins with injury to endothelial cells. This injury can occur upon exposure to many injurious agents such as high levels of low density lipoprotein cholesterol (LDL-C), hypertension, diabetes mellitus, and tobacco smoke as well as infectious agents. Once the injury occurs, lipoproteins and inflammatory cells are attracted to the area. Activated macrophages and T lymphocytes contribute to the inflammatory process and release cytokines into the circulation attracting further inflammatory cells to the area of injury. Many of these inflammatory cytokines can be measured in the plasma and correlate with both the extent of coronary disease and complications of the disease.
Background and Objective Previous study showed tenecteplase and alteplaxe were equovalent for 30-day mortality in the treatment of acute myocardial infarction. The purpose of this open-label, randomized, multi-center, angiographic trial was to assess the efficacy and safety of tenecteplase compared with alteplase in Chinese patients with acute myocardial infarction. Methods We recruited patients with acute ST-elevation myocardial infarction presenting within 6 hours of symptom onset from October, 2002 to March, 2004, in 5 hospitals in Beijing. After giving informed consent, patients were randomly assigned a single-bolus injection of tenecteplase (30-50 mg according to body weight) or front loaded alteplase (100 mg), and underwent coronary angiography at 90 min after starting the study drug. All patients received aspirin and heparin (target activated partial thromboplastin time 50-70 s). The primary efficacy end point was the rate of TIMI grade 3 flow at 90 minutes. Other efficacy end points included TIMI grade 2/3 flow at 90 minutes. Safety end points included all stroke, intracranial hemorrhage (ICH), moderate/severe hemorrhage (except for ICH), all-cause mortality at 30-days, and major non-fatal cardiac events at 30 days. Results Overall 110 patients were eligible for statistical analysis, with 58 patients assigned to receive tenecteplase and 52 patients to alteplase. Tenecteplase produced a rate of TIMI grade 3 flow at 90 minutes after the start of thrombolysis (68.4%) similar to that of alteplase (66.7%, P=1.0); the rates of TIMI grade 2 or 3 were similar for patients treated with tenecteplase versus alteplase (89.5% versus 80.4%, respectively, P=0.278). At 30 days, rates for all strokes were similar for the two groups (5.17% for tenecteplase and 1.92% for alteplase, P=0.62); rates of ICH were 3.45% and 1.92% (tenecteplase and rt-PA, P=1.00) respectively. The rate of moderate/severe hemorrhage was 8.62% with tenecteplase and 5.77% with alteplase (P=0.72); total mortality was almost identical in the two groups (13.8% versus 9.6%, respectively, P=0.565) while the rates of non-fatal cardiac complications were 10.35% and 11.54% (tenecteplase and alteplase￡?P=1.0). Conclusions The efficacy of a single-bolus, weightadjusted tenecteplase fibrinolytic regimen is equivalent to front-loaded alteplase in terms of the rates of TIMI grade 3 flow, and TIMI 2 or 3 flow, but the 30-day mortality and ICH in both groups was so high that the use of tenecteplase is not permitted in China. These negative safety results might be due to the high rate of percutaneous coronary intervention (PCI) and high dose of bolus heparin and suboptimal concomitant medical therapy during hospitalization, so further studies are needed to confirm the safety for tenecteplase in Chinese patients.
Following ST-segment elevation myocardial infarction (STEMI), early and complete epicardial reperfusion is associated with improved survival.1 For decades, the only available pharmacologic intervention aimed at reperfusion was intravenous streptokinase (SK). The efficacy of (SK) was firmly established in the Italian Group for the Study of Streptokinase in Myocardial Infarction (GISSI-1) trial, which reported an 18% relative reduction in mortality among patients presenting with STEMI within 12 hours after the onset of symptoms.2 Despite the fact that tissue-plasminogen activator (t-PA) is associated more rapid dissolution of thrombus,3 three large-scale clinical trials did not report a difference in mortality between SK and alteplase t-PA.4-6 It took altering the method of administration of alteplase t-PA, so-called front-loading (i.e. two-thirds of the dose over the first 30 minutes and the remaining dose over 60 minutes) rather than a 3-hour infusion, to lower mortality by about 1% with alteplase t-PA over SK.7 The drawback of alteplase t-PA was a small but significant increase in the risk of hemorrhagic stroke.
Objective To investigate the impact of simvastatin on blood lipid and the incidence of atrial fibrillation and ischemic-related events in patients with acute myocardial infarction accompanied by paroxysmal atrial fibrillation. Methods One hundred and three patients with acute myocardial infarction and paroxysmal atrial fibrillation were selected as subjects, and were divided into a simvastatin group and a control group. Forty-five patients were in the simvastatin group, who took simvastatin 20mg/d orally for 18 months; fiftyeight patients were in the control group, and received conventional therapy except for statins. All patients were followed up for 18 months. The level of blood lipid, recurrence rate of paroxysmal atrial fibrillation, incidence rate of persistent or permanent atrial fibrillation, and the ischemic-related events were investigated and compared between the two groups. Results ①The levels of blood lipids did not change significantly in the control group (P>0.05); concentrations of total cholesterol (TC) and low density lipoprotein cholesterol (LDL-C) decreased significantly after treatment of simvastatin (P<0.05). ② Recurrence of atrial fibrillation was observed in five patients during 18 months follow-up in the simvastatin group (11.1%), whereas it occurred in 14 patients of the control group(24.1%, P<0.05); the occurrence rate of persistent or permanent atrial fibrillation in the simvastatin group was 4.4%, which was lower than that of control (12.1%, P<0.05). ③ Nine patients had ischemic-related events in the simvastatin group (20.0%), with three heart failures (6.6%), two rehospitalizations for deterioration of coronary heart diseases (4.4%), three cardiac deaths (6.6%), and one cerebral stroke (2.2%), which was lower evidently than in the control group (41.4%, P<0.05). Conclusions Simvastatin can not only decrease the levels of serum TC and LDL-C but also prevent the occurrence of atrial fibrillation and ischemic-related events.
In the long term effects of simvastatin on protecting against atrial fibrillation in patients with acute myocardial infarction, in this issue of the Journal of Geriatric Cardiology, Chi et al. presented interesting data regarding the positive beneficial effects of simvastatin in the reduction of the frequency of atrial fibrillation in a selected group of patients. There have been occasional reports suggestive of mild antiarrhythmic properties of simvastatin, but these were more observational in nature. What is thought provoking about this report is that the group receiving simvastatin actually received less beta blocker therapy than the control group. It remains unclear as to how simvastatin actually reduces dispersion of tissue refractoriness, the basis of most arrhythmias. It also remains unclear as to whether there is a class effect (statin as a class having an effect in atrial fibrillation suppression), or whether this is specific to simvastatin alone. Patients included in this study all had acute myocardial infarction. It remains to be seen if this apparent antiarrhythmic property of simvastatin (or other statins) can be seen in other patients with atrial fibrillation and without organic heart disease. Clearly, atrial fibrillation is a heterogeneous condition, with many different etiologies, and presentations, and no single intervention is expected to be the single answer for all cases. Nonetheless the data in this study are indeed thought provoking and may add one more therapeutic option to what is presently available for the treatment of the most common arrhythmia.
Objective To investigate the effects of telmisartan on the blood glucose, blood lipid, blood insulin, and insulin resistance in the hypertensive patients with dyslipidemia, and also its effect on controlling blood pressure. Patients and Methods A total of 96 hypertensive patients (34 females, 62 males) with dyslipidemia were included (mean age 51.2±9.6, range 42-65 years). Patients were randomized to receive either telmisartan 80 mg/day (n=46) or enalapril 10 mg/day (n=50) for 6 months. The levels of blood pressure (BP), heart rate (HR), and biochemical data were measured before therapy and at the end of the 3-month treatment and 6-month treatment, respectively. Meanwhile, insulin resistance was evaluated by using a homeostasis model assessment of insulin resistance (HOMA-IR) and insulin sensitivity (HOMA-IS). Results In the telmisartan group, the mean blood pressure was obviously lower than that of pre-therapy (P< 0.05), and the levels of triglyceride (TG), HOMA-IR, and HOMA-IS were all obviously lower than those of pre-therapy and of the enalapril group at the end of the 3-month-treatment period (P<0.05). After 6 months of treatment, the levels of TG, HOMA-IR, and HOMA-IS in the telmisartan group were significantly lower in comparison with those of pre-therapy, the enalapril group (P<0.01), and 3-month-treatment (P<0.05). Post-prandial12 hour blood glucose (P2HBG) in the telmisartan group decreased significantly after 6-month treatment compared with that of pre-therapy and the enalapril group (P<0.05). The level of high density lipoprotein (HDL) cholesterol was significantly higher after 6-month treatment in the telmisartan group than with pre-therapy and the enalapril group(P<0.05). Conclusions Telmisartan could not only control blood pressure steadily and effectively, but also decrease blood TG, increase HDL cholesterol and insulin sensitivity, and lower insulin resistance.
The benefits of angiotensin converting enzyme inhibitor (ACEI) and angiotensin receptor blocker (ARB) beyond blood pressure reduction have been proven through many large studies (HOPE, LIFE) in high risk CVD patients;1 post hoc studies have shown reductions in new onset type 2 diabetes mellitus (DM). However, there are no studies which revealed a strong correlation between impaired fasting glucose (IFG) and cardiovascular disease (CVD); instead, there were correlations with post challenge glucose and post challenge insulin levels. Insulin resistance (IR) is fundamental to high risk CVD situations and high fasting and post challenge insulin levels are surrogate markers for IR, albeit inconsistently. A logical approach to the prevention of type 2 DM and CVD must be therapeutic insulin reduction. Type 2 DM clearly influences the incidence of poor outcomes in CVD patients, and for any level of risk factors analyzed, a mechanism or mechanisms unique to or heavily represented by type 2 DM/impaired glucose tolerance (IGT)/IFG/metabolic syndrome (MetS) makes subjects more prone to CVD.2 Hyperglycemia is the most prevalent feature in DM, hence it is reasonable to assume that it is an independent risk factor for CVD which could be controlled by euglycemia.
Objective To assess the prevalence and risk of coronary artery disease (CAD) in Chinese adults with type 2 diabetes mellitus (T2DM) using electron beam computed tomography (EBCT) and EBCT angiography (EBCTA). Methods: Ninety-four cases were enrolled in this study including diabetes (n=28), impaired glucose tolerance (IGT, n=30), coronary heart disease (CHD, n=11), and control (n=25). Cardiac EBCT plain scanning and EBCTA were performed on all of these subjects to evaluate coronary artery calcification (CAC) scores, and number of segments of stenosed coronary arteries. Both CAC and/or coronary artery stenosis were defined as patients with coronary artery lesions (CAL). Results CAC scores were not different with the control, diabetes, IGT, or CHD (P>0.05) groups. Compared to control (0.520±1.295), more stenosed coronary arteries segments (P<0.05) were detected in diabetes (2.964±1.915), IGT (2.200±2.024), and CHD (2.273±1.679). Number of stenosed artery segments were correlated with age (r=0.215, P=0.019), postprandial glucose (r=0.224, P=0.015), total cholesterol (r=0.323, P=0.000), and duration of diabetes (r=0.208, P=0.004). The incidences of CAL in diabetes (96.43%), IGT (93.33%), and CHD (90.91%) was substantially higher than that in normal control (56.00%, P<0.01). The odds ratio of CAL associated with having diabetes was estimated to be 7.514 (95% CI: 1.885-63.778). Conclusions Coronary artery lesions are prevalent in Chinese adults with type 2 diabetes, implying a high CAD risk. EBCTA holds potential in depicting the details of CAL and can be used to track the progression of CAD in diabetes patients.
In this issue of the Journal of Geriatric Cardiology, Huang et al. have reported the detection of coronary artery disease with electron-beam computed tomography (EBCT), utilizing non-contrast and contrast imaging techniques (EBCTA) in several subgroups including type 2 diabetes mellitus (DM), impaired glucose tolerance (IGT), coronary heart disease, and normal subjects. Interestingly, non-contrast imaging by measurement of the coronary artery calcium score (CAC) did not show any differences among the groups. However, the presence of coronary calcification and/or coronary stenotic lesions detected by contrast coronary angiography with EBCTA was found more frequently in type 2 DM, IGT, and coronary artery disease patients than in healthy subjects. The authors concluded that combined information on either CAC or luminal assessment with EBCTA should be considered for assessment of atherosclerosis in type 2 DM patients.
Tumors of the cardiac conduction system (CCS) have rarely been reported. The CCS from 198 cardiac-related deaths (Group Ⅰ), and 838 deaths from non-cardiovascular diseases or trauma (Group Ⅱ), were studied. Sampling was done of the sinoatrial node (SAN) and atrio-ventricular node (AVN) along their long axis of each node as a single block and the His bundle (HB) perpendicular to its long axis in 2-4 blocks. Five-micron serial sections were made; tissue slices were taken intermittently, every 20th from the SAN, every 10th from the AVN, and every 30th from the HB and bundle branches (BB), by continuous slices three times. Tumors in the CCS were found in 12 cases (1.155 %), where 10 (0.965%) were primary tumors, and 2 (0.193%) were metastatic tumors. The primary tumors included 4 fibromata compressing the HB (0.386 %), 4 hemangiomata (0.386%), 1 AVN tumor (0.097 %), and 1 rhabdomyoma (0.097 %). In 8 of the 10 cases, the tumors were located in the AVN or HB. The metastatic tumors originated from lymphocytic leukemia and malignant lymphoma (histiocytic type) in lung, and were all found in the SAN. Of the 12 cases, 2 were from the group ￠?. Tumors in the CCS are the smallest tumors in different parts of the body, which can cause sudden death.
Cardiac tumors are well described in the literature. The first reports of cardiac tumors date back hundreds of years. The prevalence of primary cardiac tumors at autopsy ranges from 0.001% to 0.3% with secondary tumors more common than in primary tumors.
Objective Dilated cardiomyopathy (DCM) is generally considered to be accompanied by both left and right ventricular dysfunction, but most studies only analyze the left ventricular function. In this study, we evaluated the effect of arotinolol on right ventricular function in patients with DCM. Methods Right ventricular ejection fraction (RVEF) and right ventricular diameter (RVD) were measured by two-dimensional echocardiography (2-DE) in 33 DCM patients; RVEF measured by first-pass radionuclide angiography (FPRA) was compared with that by 2-DE. Results The treatment with arotinolol for one year resulted in a reduction in the right ventricular diameter (baseline, 23.0±8.3 mm vs after one-year treatment, 20.7±5.4 mm; P=0.004 ) and an associated increase in ejection fraction (baseline, 36.9±10.3% vs after one-year treatment, 45.8±9.6%; P < 0.001 ); there is a high correlation between the 2-DE method and radionuclide ventriculographic method. The correlation coefficient is 0.933 (P<0.001). Conclusion Arotinolol therapy could not only improve left ventricular function, but also improve right ventricular function in DCM patients.
In this issue of the Journal of Geriatric Cardiology,Yang et al.1 studied the effects of arotinolol, a beta-blocker (BB), on the right ventricular (RV) function. (1) In the past, most studies were focusing on the left ventricle (LV) because the RV was considered only a passive conduit. (2) This study follows a new path in searching for a comprehensive understanding of RV function with possible pro-active and aggressive interventions in RV dysfunction and failure.
Objective To investigate the mechanism of ventricular dilation-induced arrhythmias by dilating isolated rat hearts. Methods Isolated rat hearts were perfused by Langerdorff method. After equilibration, 80 hearts were randomly divided into four groups as follows: (1) control group (n=20), (2) Ca2+ preconditioning (CPC) group (n=20), (3) streptomycin group (n=20), and (4) CPC + streptomycin group (n=20). A latex balloon which can be filled with fluid was anchored in the left ventricle through the left atrium and mitral valve. Epicardial ECG of the left ventricle, left ventricular pressure, coronary flow and heart rate were recorded before and during ventricular dilation by injecting fluid into the latex balloon. The rate and duration of ventricular dilation-induced arrhythmias were recorded. Results Under the same increase in ventricular end-diastolic pressure made by inflation of the balloon, the rate of arrhythmias was 100% and duration of arrhythmias was 2. 56±0.46s in the control group. Both the rates of premature ventricular beat (90%)and ventricular tachycardia 70%)were high. Compared with the control group, the total rate (60%) of arrhythmias was lower, and duration(1.67±0.61s)of arrhythmias was shorter in the CPC group. Both the rates of premature ventricular beat (60%)and ventricular tachycardia (40%) were low comparatively. The rate of arrhythmias (45%)was lower and duration (1.64±0.42s)of arrhythmias was shorter, and the rates of premature ventricular beat (30%) or ventricular tachycardia (35%)were lower in the streptomycin group than in the control one. The least ventricular dilation-induced arrhythmias occurred in the CPC + streptomycin group. The rate of arrhythmias(10%)was the lowest and duration (1.01±0.37s)of arrhythmias was the shortest; both the rates of premature ventricular beat(5%) and ventricular tachycardia (10%)were the lowest. Conclusions Ventricular dilation may induce arrhythmias in isolated rat hearts. Stretch-activated ion channel and the increase in [Ca2+]i are supposed to play important roles in the pathological mechanism.
In this issue of the Journal of Geriatric Cardiology, Yin et al discussed the effects of calcium preconditioning (CPC) and streptomycin (S) on acute dilation of the left ventricle.
Slow coronary flow phenomenon(SCFP) is an angiographic observation characterized by delayed distal vessel opacification in the absence of significant epicardial coronary disease. Only limited studies have been focused on the etiologies, clinical manifestations and treatment of this unique angiographic phenomenon. In our case report, we described an 85-year-old man who came with significant ST segment elevation in leads V1-V4 and V3R-V5R without increase in myocardial enzyme. The patient also developed respiratory failure requiring intubation and mechanical ventilation. Coronary angiography revealed only mild atherosclerosis without spasm or thromboembolic occlusion. Slow flow was seen in all coronary arteries, especially in the left anterior descending and right coronary arteries. This case speculated that transmural myocardial ischemia with ST segment elevation might be resulted from slow coronary flow. Transmural myocardial ischemia can occur owing to abnormalities of the coronary microcirculation.
Elderly patients with myocardial infarction commonly present with symptoms other than chest pain. The clinician evaluation of the elderly may rely on laboratory methods more so than in younger patients. Fortunately, advances in laboratory science have brought newer biomarkers of cardiac injury to the clinical arena including cardiac troponins I and T(cTnI,cTnT). These regulatory components of the contractile apparatus are sensitive indicators of myocardial injury. Their central role in the current definition of acute myocardial infarction highlights their utility in the diagnosis of acute myocardial ischemic syndromes. The troponins are also released in some clinical situations where thrombotic complications of coronary artery disease and resultant acute myocardial infarction have not occurred. Examples of these conditions include conditions like myocarditis, pulmonary embolism, sepsis, and acute stroke. Elevated troponins in these conditions are thought to emanate from injured myocardial cells and in most circumstances have been associated with adverse outcomes. Interpretation of elevated troponin in the elderly requires consideration of other possible conditions.