Correlation between myocardial enzyme serum levels and markers of inflammation with severity of coronary artery disease and Gensini score: A hospital-based,prospective study in Greek patients

Background

Our objective was to associate serum levels of myocardial enzymes and inflammatory biomarkers with severity of coronary artery disease (CAD).

Patients and methods

123 patients participated in our study, including 65 cases of acute myocardial infarction (MI), 27 cases of newly diagnosed CAD – without MI – and 31 controls. In all subjects, myocardial serum enzyme levels (creatine phosphokinase, aspartate aminotransferase, lactate dehydrogenase) and inflammatory indices (C-reactive protein, fibrinogen, white blood cells, and erythrocyte sedimentation rate) were measured. Patients were all submitted to coronary angiography and CAD severity was evaluated by Gensini score.

Results

Significant differences concerning enzyme serum levels and inflammatory indices were found to exist between the three study groups, being highest among patients with acute MI (p < 0.001). A significant association was demonstrated between Gensini score and serum enzyme levels as well as inflammatory biomarkers.

Conclusions

Our findings suggest that serum levels of myocardial enzymes and inflammatory indices correlate with CAD severity in Greek patients.     

钙调神经磷酸酶信号通路在心肌肥厚中的作用

心肌肥厚是许多心血管病的病理结果,可引起心力衰竭,增加猝死发生率。因此,探讨心肌肥厚发生机制,寻求延缓和治疗心肌肥厚的新途径,早已引起人们的重视。近年来,研究发现钙调神经磷酸酶(Ca2 /钙调素调节的丝氨酸/苏氨酸蛋白磷酸酶)可通过多种信号通路参与心肌肥厚的形成。现综述钙调神经磷酸酶信号通路在心肌肥厚发展中的作用。     

Absence of inferior vena cava as a rare cause of deep venous thrombosis complicated by liver and lung embolism

Congenital anomalies of the inferior vena cava such as absence or atresia are uncommon vascular defects and result from aberrant development during embryogenesis. We report a case of a young female patient affected by proximal deep venous thrombosis (DVT) complicated by liver and pulmonary embolism; subsequent extensive evaluation revealed the congenital absence of infrarenal inferior vena cava, with emboli probably occurring through collateral veins. Accordingly, in young patients with idiopathic DVT of the lower extremities and pelvic veins, the presence of inferior vena cava abnormalities should always be considered and investigated, together with classic coagulation factors, as a factor predisposing to thromboembolic complications.     

Angiographically evident thrombus following fibrinolytic therapy is associated with impaired myocardial perfusion in STEMI: a CLARITY-TIMI 28 substudy.

AIMS: The presence of residual thrombus following fibrinolytic therapy for ST-segment elevation myocardial infarction (STEMI) may predispose to greater embolization and microvascular dysfunction. METHODS AND RESULTS: We hypothesized that even in the presence of a patent epicardial artery, residual thrombus would be associated with worsened TIMI myocardial perfusion grades (TMPG), independent of epicardial flow. Data were analysed from the angiograms of 2684 patients enrolled in the CLARITY-TIMI 28 trial, with angiographically patent arteries (TIMI 2/3 flow) at a median of 88 h following fibrinolytic therapy. Thrombus in a patent epicardial artery was observed more frequently among patients with shorter times from randomization to angiography, among patients with non-left anterior descending infarctions, and among patients treated with placebo (vs. clopidogrel). Thrombus was associated with more frequent TIMI 2 flow (35.1 vs. 22.1%, P < 0.001), higher corrected TIMI frame counts (CTFC) (42 vs. 33 frames, P < 0.001), and a lower incidence of normal TMPG 3 (48.7 vs. 63.9%, P < 0.001), irrespective of treatment with clopidogrel or placebo. In multivariable analyses, thrombus remained associated with higher CTFC (P < 0.001) and worse TMPG (OR 1.6 for TMPG 0/1/2, P < 0.001) after adjustment for baseline covariates as well as known correlates of TMPG. The association between thrombus and impaired TMPG remained even after further adjustment for CTFC or TIMI flow grade. CONCLUSION: Residual angiographic thrombus following fibrinolytic therapy in STEMI patients is associated with impaired myocardial perfusion, independent of epicardial flow. This finding emphasizes the roles of platelet aggregation and distal embolization in the pathogenesis of microvascular dysfunction in STEMI.     

Late QRS Activity in Signal‐Averaged Magnetocardiography,Body Surface Potential Mapping,and Orthogonal ECG in Postinfarction Ventricular Tachycardia Patients

Background: Delayed electrical activity necessary for re‐entrant ventricular tachycardia (VT) is detectable noninvasively with high resolution techniques. We compared high resolution signalaveraged analysis of magnetocardiography (MCG), body surface potential mapping (BSPM), and orthogonal three‐lead ECG (SA‐ECG) in the identification of patients prone to VT after myocardial infarction (Ml). Methods: Patients with remote myocardial infarction and cardiac dysfunction were studied, 22 with (VT group) and 22 without VT (control group). MCG with seven channels and BSPM with 63 and SA‐ECG with three orthogonal leads were registered. After signal‐averaging and highpass filtering, three time domain analysis (TDA) parameters describing late electrical activity were computed: QRS duration (QRSd), root mean square amplitude (RMS) of the last 40 ms of QRS, and the duration of the low‐amplitude QRS end (LAS). Results: All parameters by each method were significantly different between the patients’groups. For example, LAS parameter in MCG was 59 (SD 22) ms in the VT group vs. 37 (SD 13) ms in controls (P < 0.001), 77 (SD 22) ms vs. 56 (SD 19) ms in BSPM (P = 0.002), and 60 (SD 24) ms vs. 39 (SD 22) ms in SA‐ECG (P = 0.005). The combination of LAS parameter in MCG and SA‐ECG resulted in improved performance in comparison to any single parameter with 95% sensitivity and 68% specificity. Conclusions: All three high resolution methods identified VT propensity among post‐Mi patients with cardiac dysfunction and between‐method differences were small. Information in MCG and SA‐ECG may be complementary and their combination could be of value in postinfarction arrhythmia risk assessment. A.N.E. 2002;7(4):389–398     

复跳前控制性温血停跳液灌注的心肌保护作用

目的探讨复跳前自体氧合温血停跳液控制性灌注在体外循环手术中对心肌缺血再灌注损伤的保护作用.方法选择256例复杂或重症患者,随机分为对照组128例,实验组128例.常规在体外循环下进行各种手术,均采用4℃ThomasⅡ号液间断顺灌行心肌保护.实验组在主动脉开放前约5min,用4:1自体氧合温血停跳液控制性灌注(压力:50mmHg,量:10ml/kg,流量:100～200ml/min,温度:35℃).分别在阻断主动脉前和开放主动脉后0,1,6,24h测定心肌酶,比较二组自动复跳率、复跳后血流动力学、围术期升压药应用、心律失常发生率、病死率、术后心功能等指标.结果实验组心肌酶含量低于对照组(P＜0.05),其余各指标优于对照组(P＜0.05).结论复跳前控制性温血灌注对心肌缺血有良好保护作用,方法简单、可行,值得临床应用.     

Dual‐Dye Optical Mapping after Myocardial Infarction: Does the Site of Ventricular Stimulation Alter the Properties of Electrical Propagation?

Introduction: Myocardial infarction (MI) disrupts electrical conduction in affected ventricular areas. We investigated the effect of MI on the regional voltage and calcium (Ca) signals and their propagation properties, with special attention to the effect of the site of ventricular pacing on these properties.
Methods: New Zealand White rabbits were divided into four study groups: sham-operated (C, n = 6), MI with no pacing (MI, n = 7), MI with right ventricular pacing (MI + RV, n = 6), and MI with BIV pacing (MI + BIV, n = 7). At 4 weeks, hearts were excised, perfused, and optically mapped. As previously shown, systolic and diastolic dilation of the LV were prevented by BIV pacing, as was the reduction in LV fractional shortening.
Results: Four weeks after MI, optical mapping revealed markedly reduced action potential amplitudes and conduction velocities (CV) in MI zones, and these increased gradually in the border zone and normal myocardial areas. Also, Ca transients were absent in the infarcted areas and increased gradually 3–5 mm from the border of the normal zone. Neither BIV nor RV pacing affected these findings in any of the MI, border, or normal zones.
Conclusions: MI has profound effects on the regional electrical and Ca signals and on their propagation properties in this rabbit model. The absence of differences in these parameters by study group suggests that altering the properties of myocardial electrical conduction and Ca signaling are unlikely mechanisms by which BIV pacing confers its benefits. Further studies into the regional, cellular, and molecular benefits of BIV pacing are therefore warranted.     

WBC、IL-6对急性心肌梗死患者近期预后的影响

目的 观察急性心肌梗死（AMI）患者人院外周血白细胞（WBC）总数、血浆白细胞介素-6（IL-6）对近期预后的影响。方法 首发AMI患者103例，通过检测WBC、IL-6，以发病后30天内是否发生心血管不良事件（包括心源性死亡、心力衰竭、心源性休克、恶性心律失常）为观察终点。结果 36例发生心血管事件组外周血WBC总数和IL-6显著高于67例无心血管事件组。AMI时外周血WBC总数和IL-6水平为发生心血管事件的预测因素。结论 WBC、IL-6与AMI患者近期预后相关。     

急诊经皮冠状动脉介入、溶栓和常规药物治疗对急性心肌梗死的疗效分析

目的评价急诊经皮冠状动脉介入治疗(PCI)、静脉溶栓和常规药物治疗对急性心肌梗死(AMI)疗效的对照分析。方法114例AMI患者,其中PCI组42例,溶栓组38例,药物组34例,分别收集患者治疗前和治疗2h、4h、8h、24h、72h静脉血,检测心肌酶谱和肌钙蛋白变化以及心电图ST段回降情况。结果①PCI组在手术后8h心肌酶和肌钙蛋白提前达到高峰,与其他组比较有显著差异(P<0.01)。72h后PCI组绝大多数心肌酶和肌钙蛋白已恢复正常,而其他组心肌酶和肌钙蛋白仍维持较高水平;②PCI组在治疗后8hST段已有较大回落,其余组ST段回落不明显,3组比较有显著差异。72hPCI组ST段已恢复正常,而其余组仍然较高,3组比较有显著意义(P<0.01)。结论急诊PCI能使AMI患者心肌酶峰迅速提前,且短时间恢复正常,此外,使肌钙蛋白、心肌酶、心电图ST段较短时间内恢复正常。     

Contractile dysfunction in hypertrophied hearts with deficient insulin receptor signaling: possible role of reduced capillary density

Diabetics have worse outcomes than nondiabetics after a variety of cardiac insults. We tested the hypothesis that impaired insulin receptor signaling in myocytes worsens cardiac remodeling and function following injury, even in the absence of hyperglycemia. Mice with cardiomyocyte-restricted knock out of the insulin receptor (CIRKO) and wild type (WT) mice were treated with isoproterenol (ISO) for 2 or 5 days. Heart rates and cardiac mass increased comparably following ISO in WT and CIRKO mice. After 5 days, WT hearts were hyperdynamic by echocardiographic and left ventricular pressure measurements. However, CIRKO hearts had a blunted increase in contractility and relaxation following ISO. Interestingly, single myocytes isolated from both CIRKO ISO and WT ISO hearts had increased cellular shortening with prolonged time to peak shortening vs. respective shams. Thus, loss of myocytes or extramyocyte factors, rather than intrinsic dysfunction of surviving myocytes, caused the blunted inotropic response in ISO treated CIRKO hearts. Indeed, CIRKO ISO mice had increased troponin release after 2 days and greater interstitial and sub-endocardial fibrosis at 5 days than did ISO WT. Apoptosis assessed by TUNEL and caspase staining was increased in CIRKO ISO compared to WT ISO hearts; however, very few of the apoptotic nuclei were clearly in cardiac myocytes. After 5 days of ISO treatment, VEGF expression was increased in WT but not in CIRKO hearts. In keeping with this finding, capillary density was reduced in CIRKO ISO relative to WT ISO. Basal expression of hypoxia-inducible factor-1alpha was lower in CIRKO vs. WT hearts and may explain the blunted VEGF response. Thus, absence of insulin receptor signaling in the cardiac myocyte worsens catecholamine-mediated myocardial injury, at least in part, via mechanisms that tend to impair myocardial blood flow and increase ischemic injury.