Ventricular Non-Compaction: About the First Cases Reported in Lomé(Togo)

Introduction: Ventricular non-compaction, a cardiomyopathy recently described as likely to be rare, belongs to the group of unclassified cardiomyopathy according to European Society of Cardiology. Few studies have been published on the ventricular non-compaction in sub-Saharan Africa. We aim to find out the various aspects, being diagnosis, therapeutic, in Togolese patients carrying the ventricular non-compaction. Methodology: This is a three-year prospective and descriptive study conducted from January 2017 to December 2019 in the two University Hospital of Lomé. Patients having echocardiographic criteria of ventricular non-compaction were included in our study. Results: 10 patients (6 men and 4 women) were diagnosed for ventricular non-compaction during the study period. The mean age of patients was 32.3 years. The most frequent clinical manifestation was heart failure (7 patients). The main electrocardiogram anomaly was left ventricle hypertrophy (9 patients). The preferential segments were: apical (9 cases), apicolateral (8 cases), and septoapical (7 cases). The average ratio of non-compaction/compaction was 3.31. The main complication was thromboembolic event (4 patients). Angiotensin converting enzyme inhibitors and beta-blockers were essentially the medicines used. After a three (3) year follow-up, two (2) of the patients died. Conclusion: Tough ventricular non-compaction has been recently described. It is present in Togo. It displays many clinical manifestations and the prognosis is often guarded.

A Case Report of Isolated Left Ventricular Non-Compaction Presenting with Congestive Heart Failure and Intramural Thrombus

Isolated left ventricular non-compaction is recently described as a rare form of cardiomyopathy that is associated with a heart failure, life threatening cardiac arrhythmia and thromboembolic complications. The diagnosis is based on echocardiography demonstration of spongy myocardium. Here we report a case of 74 years old female patient diagnosed as an isolated left ventricular non-compaction with congestive heart failure, intramural thrombus and hypertension. There is no specific treatment for LVNC;therapeutic measures are directed towards the patient’s symptom (heart failure, arrhythmia and thrombotic events) and consideration of an implantable cardioverter defibrillator and cardiac transplantation.

Effects of PPAR-y in the Myocardium on the Development of Ventricular Septation

Ventricular septum defects(VSDs)are common types of congenital heart diseases caused by developmental defect;they contribute to 25%-30%of all adult congenital heart diseases.The peroxisome proliferator-activated receptor gamma(PPAR-y)is widely expressed in mammalian tissues and in the immune system,regulating cell differentiation and immune and inflammatory responses.The PPAR-y gene has recently been found crucial for heart development,but the mechanism of action is not clear.This study aims to investigate the effects of the PPAR-y gene in the myocardium on the development of ventricular septation.In this study,we applied Cre-loxP recombination enzyme(CRE)technology to downregulate the expression of the PPAR-y gene in different cardiac tissues,RT-PCR to examine the expression of the c-fos and TGF-B!genes,and histology staining to check the defect of embryonic heart at embryonic day 14.5(E14.5).We found that the downregulation of the PPAR-p gene resulted in a ventricular membranous septation defect of the embryonic heart at E14.5.Furthermore,only conversion of a Tnt:Cre,but not Mef2c:Cre,Tie2:Cre,or Wnt:Cre PPAR-T floxed allele to a null allele resulted in VSD.PPAR-/mi-Orv+embryos showed increascs in atrioventricular(AV)-cushion cells and the expression of c-fos gene but no change in the expression of TGF-B1 at E10.5.Our study demonstrates PPAR-N in the myocardium is required for ventricular septation through regulation of AV-cushion cell proliferation by a Tntc-fos signal.

A Case of Recurrent Multiple Left Ventricular Thrombi without Thromboembolism in Noncompacted Myocardium

Background: Left ventricular noncompaction with multiple left ventricular thrombi can be revealed by echocardiography, and early diagnosis seems to be imperative to prevent significant embolic events. Case Report: A 57-year-old woman presented with symptoms of heart failure. Two-dimensional transthoracic echocardiogram demonstrated a dilated and diffusely hypokinetic left ventricle with severe impaired left ventricular systolic function. Moreover, a markedly thickened endocardium at the left ventricular apex and middle segment with numerous, excessively prominent trabeculations and deep intertrabecular recesses were present. During systole, the ratio of the noncompacted to compacted myocardial layers at the site of the maximal wall thickness was above two, a characteristic finding in left ventricular non-compaction. Multiple mobile, homogeneous, echodense thrombi were identified in the left ventricle, with the largest one in the apical noncompacted segment (dimensions, 32 × 14 mm). Cardiac magnetic resonance imaging confirmed the diagnosis of noncompacted myocardium with the presence of multiple thrombi. After anticoagulant therapy, her symptoms improved and thrombi dissolved. Unexpectedly, she re-admitted to the cardiovascular unit with progressive dyspnea. Transthoracic echocardiogram showed new large right atrial thrombi, with the largest one was 43 × 38 mm compared to the echocardiogram done 11 months ago. The patient was anticoagulated with continuous heparin infusion for several days followed by oral Apixaban. After 4 weeks, the floating thrombi completely disappeared. After a 26-month follow-up, the patient’s condition was stable without embolic complications. Conclusion: Echocardiography was the cornerstone of diagnostic methods for early detecting left ventricular thrombi to eventually prevent embolic events.

The Relation Between Hypertrophied Myocardium and Ventricular Fibrillation Threshold in Spontaneously Hypertensive Rats

Objectives To investigate the relation between hypertrophied myocardium and ventricular fibrillation threshold in spontaneously hypertensive rats （SHR）. Methods 20 male SHR were randomly divided into two groups： 10 week group （n= 10） and 18 week group （n=10）. 10 week male Wistar rats were controlled group （n=10）. The systolic blood pressure （SBP）, heart mass index （HMI）, ventricular effective refractory period （VERP） and ventricular fibrillation threshold（VFT） were measured respectively.① The SBP and HMI of SHR were significantly higher than those of Wistar rats（P 〈 0.001）. The VFT of SHR were significantly lower than that of Wistar rats （P 〈 0.001）.②In SHR, the SBP and HMI of 18 week SHR were significantly higher than those of 10 week SHR （P 〈 0.001）. The VFT of 18 week SHR were significantly lower than that of 10 week SHR （P 〈 0.001）. ③There were no significant difference of VERP among 10 week SHR, 18 week SHR and Wistar rats（P 〉 0.05）. ④There was no relationship between HMI and VFT or SBP in Wistar rats. There was significant relationship between HMI and VFT or SBP in different age spontaneously hypertensive rats. ⑤HMI, age and species of animal were the major influent factors of VFT. Conclusions The VFT of hypertrophied myocardium decreased. The higher the degree of hypertrophy of myocardium and the higher the systolic blood pressure were, the lower the ventricular fibrillation threshold was.

Viable Myocardium Impact on Left Ventricular Function after Late Revascularization of Infarct-related Artery in Acute Myocardial Infarction

Objectives The long-term benefit of late reperfusion of infarct-related artery （IRA） after acute myocardial infarction （AMI） is controversial, and the benefit mechanisms remain uncertain. Low dose dobutamine stress echocardiography （LDSE） can identify viable myocardium and predict improvement of wall motion after revascularization. Methods Sixtynine patients with first AMI who did not received early reperfusion therapy were studied by LDSE at 5 to 10 days after AMI. Wall motion abnormality and left ventricular size were measured at the same time. Successful PCI were done in all patients at 10 to 21 days after AMI onset. Patients were divided in two groups based on the presence or absence of viable myocardium. Echocardiography was repeated six months later. Results There were 157 motion abnormality segments. 89 segments （57%） were viable during LDSE. 26 patients （38%） with viability and 43 （62%） without. In viable group, left ventricular ejection fraction （LVEF） was increased （P 〈 0.05）, and left ventricular end systolic volume index （LVESVI） and wall motion score （WMS） were decreased （P 〈 0.05 and P 〈 0.01） significantly at 6 months compared with baseline. But in patients without viability, LVEF was decreased （P 〈 0.01）, and LVESVI and left ventricular end diastolic volume index （LVEDVI） were increased （P 〈 0.05） significantly after 6 months, and the WMS did not changed （P 〉 0.05 ）. LVEF increased （P 〈 0.05 ） and WMS decreased （P 〈 0.05） on LDSE during acute phase in patients with viability, but they were not changed in the nonviable group. Conclusions Late revascularization of IRA in patients with presence of viable myocardium after AMI is associated with long-term preservation left ventricular function and less ventricular remodeling. Improvement of left ventricular systolic function on LDSE indicates late phase recovery of left ventricular function after late revascularization.

Accuracy of myocardial viability imaging by cardiac MRI and PET depending on left ventricular function

AIM To compare myocardial viability assessment accuracy of cardiac magnetic resonance imaging(CMR)compared to[^(18)F]-fluorodeoxyglucose(FDG)-positron emission tomography(PET)depending on left ventricular(LV)function.METHODS One-hundred-five patients with known obstructive coronary artery disease(CAD)and anticipated coronary revascularization were included in the study and examined by CMR on a 1.5T scanner.The CMR protocol consisted of cine-sequences for function analysis and late gadolinium enhancement(LGE)imaging for viability assessment in 8 mm long and contiguous short axis slices.All patients underwent PET using[^(18)F]-FDG.Myocardial scars were rated in both CMR and PET on a segmental basis by a 4-point-scale:Score 1=no LGE,normal FDG-uptake;score 2=LGE enhancement<50% of wall thickness,reduced FDG-uptake(≥50% of maximum);score 3=LGE≥50% ,reduced FDG-uptake(<50% of maximum);score 4=transmural LGE,no FDG-uptake.Segments with score 1 and 2 were categorized"viable",scores 3 and 4 were categorized as"non-viable".Patients were divided into three groups based on LV function as determined by CMR:Ejection fraction(EF),<30% :n=45;EF:30% -50% :n=44;EF>50% :n=16).On a segmental basis,the accuracy of CMR in detecting myocardial scar was compared to PET in the total collective and in the three different patient groups.RESULTS CMR and PET data of all 105 patients were sufficient for evaluation and 5508 segments were compared in total.In all patients,CMR detected significantly more scars(score 2-4)than PET:45% vs 40% of all segments(P<0.0001).In the different LV function groups,CMR found more scar segments than PET in subjects with EF<30% (55% vs 46% ;P<0.0001)and EF 30% -50% (44% vs 40% ;P<0.005).However,CMR revealed less scars than PET in patients with EF>50% (15% vs 23% ;P<0.0001).In terms of functional improvement estimation,i.e.,expected improvement after revascularization,CMR identified"viable"segments(score 1 and 2)in 72% of segments across all groups,PET in 80% (P<0.0001).Also in all LV function subgroups,CMR judged less segments viable than PET:EF<30% ,66% vs 75% ;EF=30% -50% ,72% vs 80% ;EF>50% ,91% vs 94% .CONCLUSION CMR and PET reveal different diagnostic accuracy in myocardial viability assessment depending on LV function state.CMR,in general,is less optimistic in functional recovery prediction.

Changes of Expression of Stretch-activated Potassium Channel TREK-1 mRNA and Protein in Hypertrophic Myocardium

The expression of stretch activated potassium channel TREK-1 mRNA and protein of hypertrophic myocardium was measured. Using a model of hypertrophy induced by coarctation of abdominal aorta in male Wistar rats, the expression of TREK-1 mRNA and protein was detected by using semi quantitative RT-PCR and Western blot respectively. At 4th and 8th week after constriction of the abdominal aorta , rats developed significant left ventricular hypertrophy. As compared to sham-operated group, stretch-activated potassium channel TREK-1 mRNA was strongly expressed and protein was up regulated in operation groups （P〈0.05）. It was concluded that the expression of TREK-1 was up-regulated in hypertrophic myocardium induced by chronic pressure overload in Wistar rats.

Voltage- and Use-dependent Effect of 7-chlor-benzylte-trahydropalmatine on Sodium Currents in Guinea Pig Ventricular Myocytes

The whole-cell patch-clamp technique was employed to obtain information about the voltage-dependence and kinetics of interaction of 7-chlor-benzylte-trahydropalmatine (7-Cl-BTHP) with cardiac sodium channels. 7-Cl-BTHP (30 mol/L) significantly decreased the peak sodium current (from 7. 8±1. 8 nA to 5. 3±1. 4 nA, P<0. 01, n=5), without producing a shift of the current-voltage curve. It shifted the inactivation curves of sodium current to hyperpolarized potentials, and the V(0.5) was shifted from - (82. 5±2. 5) mV to - (95±2.4) mV (P <0. 05, n=4). 7-Cl-BTHP produced a significant use-dependent effect that was proportional to the duration of the voltage step. In addition, 7-Cl-BTHP slowed the recovery of sodium channel from inactivation, which could explain its use-dependent effects on sodium current. The characteristics of 7-Cl-BTHP blockage suggest that this agent binds preferentially to inactivated sodium channels.

Effects of Amiodarone on Transmural Dispersion of Ventricular Effective Refractory Periods across Myocardial Layers in the Normal and Hypertrophic Canine Heart

The effects of amiodarone on transmural dispersion of ventricular effective refractory periods （ERPs） in the normal and hypertrophic canine heart were investigated in vivo. By using the programmed stimulation protocol, the ERPs of epicardium （Epi）, midmyocardium （Mid） and endocardium （Endo） were measured by inserting specially-designed electrodes into the three myocardial layers before and after mainlining of amiodarone. No significant ERPs-dispersion was observed in the three layers before and after mainlining of amiodarone in the normal group. In contrast, ERPs of all the three layers were prolonged in the hypertrophic heart, while the ERPs-dispersion was reduced significantly after mainlining of amiodarone. The ERPs-dispersion was significantly increased in the hypertrophic heart but not in the normal heart using ＂long-short＂ and ＂short-long＂ interval stimulation technique. It was concluded that （1） the differences in ERPs-dispersion among the three layers were significant in hypertrophic heart, and differences were not significant in normal canine heart; （2） ERPs of each three-myocardial layers were significantly prolonged after using amioda- rone, but the ERPs-dispersion decreased in hypertrophic heart and （3） the programmed extrastimulus technique of ＂long-short＂ and ＂short-long＂ intervals increased the transmural ERPs-dispersion in the hypertrophic heart.

昼夜节律紊乱通过影响心肌脂代谢对心肌梗死后心脏重构影响机制的相关性研究

目的探究昼夜节律紊乱是否加重心肌梗死(MI)后心脏重构及潜在的脂代谢相关机制。方法选取18只健康SPF级雄性SD大鼠,随机分为假手术(sham)组、MI组和昼夜节律紊乱(MI+Dis)组,每组6只。适应性饲养14 d后,MI组和MI+Dis组建立MI模型,MI+Dis组接受24 h持续光照7 d建立昼夜节律紊乱模型。用超声心动图评估心脏功能,苏木精-伊红染色检测MI诱导的心肌损伤,Masson染色检测心肌胶原纤维表达,免疫荧光检测心肌纤维化标志物α平滑肌肌动蛋白(α-SMA)表达,逆转录聚合酶链反应法检测肉碱棕榈酰转移酶1β(CPT-1β)、过氧化物酶体增殖物激活受体α(PPARα)、心肌胶原组织Ⅰ型(CollagenⅠ)和心肌胶原组织Ⅲ型(CollagenⅢ)的信使RNA(mRNA)表达水平,生化法检测血清三酰甘油(TG)、总胆固醇(TC)水平。结果与sham组比较,MI组大鼠左心室收缩末期内径(LVESD)、左心室舒张末期内径(LVEDD)、心肌α-SMA、CollagenⅠ、CollagenⅢ相对表达量显著升高(P<0.05,P<0.01),左心室射血分数(LVEF)和左心室短轴缩短率(LVFS)显著降低(P<0.05);与MI组比较,MI+Dis组大鼠LVESD[(8.27±0.66)mm vs(5.82±0.54)mm]、LVEDD[(10.13±0.71)mm vs(7.97±0.55)mm]、心肌α-SMA、CollagenⅠ、CollagenⅢ相对表达量、血清TG、TC显著升高(P<0.05,P<0.01),LVEF、LVFS、心肌CPT-1β、PPARα的mRNA相对表达量显著降低(P<0.05)。结论昼夜节律紊乱可能通过抑制心肌脂肪酸β氧化,扰乱心脏能量代谢稳态导致脂质堆积,加重MI后心脏重构。

Whole-exome sequencing reveals twovariants in thegene in two Chinese patients with left ventricular non-compaction cardiomyopathy

Importance:Pathogenic variants in theRBM20 gene are associated with aggressive dilated cardiomyopathy(DCM).Recently,RBM20 was found to be associated with left ventricular non-compaction cardiomyopathy(LVNC).Thus far,only five families with LVNC have been reported to carry variants inRBM20.It remains unknown whether the variants inRBM20 associated with DCM can also cause LVNC.Objective:To elucidate the causativeRBM20 variant in two unrelated patients with both LVNC and DCM,and to identify the clinical characteristics associated with variants inRBM20.Methods:Trio whole-exome sequencing(WES)was performed.Variants were filtered and classified in accordance with the guidelines of the American College of Medical Genetics and Genomics(ACMG).Results:We identified two distinctde novo variants inRBM20(one per patient)in these two patients with LVNC.Both variants have been reported in patients with DCM,without the LVNC phenotype.Patient 1 was an 11-year-old girl who had DCM,LVNC,and heart failure;the ratio of noncompacted-to-compacted myocardium was 2.7:1.Ade novo heterozygous variant c.1907G>A(p.Arg636His)in exon 9 was identified in this patient.Patient 2 was a 13-year-old boy who had clinical phenotypes identical to those of Patient 1;the ratio of noncompacted-to-compacted myocardium was 3.2:1 in this patient.WES revealed ade novo heterozygous variant c.1909A>G(p.Ser637Gly)in exon 9.Both variants were previously characterized as pathogenic,and our study classified them as pathogenic variants based on the ACMG guidelines.Interpretation:We found that two patients with LVNC had variants inRBM20.Our results extended the clinical spectrum of the twoRBM20 variants and illustrated that the same variant inRBM20 can cause DCM,with or without the LVNC phenotype.

心脏磁共振成像对急性ST段抬高型心肌梗死后左心室不良重构的预测价值

目的评估心脏磁共振(CMR)对ST段抬高型心肌梗死(STEMI)后左心室不良重构的价值。方法回顾性分析86例STEMI患者经皮冠状动脉介入术后1周及5个月的临床资料和CMR图像。所有受试者均采集电影和LGE序列。将患者分为左心室不良重构组(n=25)和无左心室不良重构组(n=61)。左心室不良重构定义为第2次CMR检查时左心室收缩末期容积(LVESV)较初始CMR增加15%或更多。CMR分析包括左心室容积、心肌梗死特征、整体和区域心肌功能。采用Logistic回归法分析左心室不良重构的独立预测因素。结果在初始CMR时,两组患者的左心室容积及左心室射血分数(LVEF)差异均无统计学意义(P>0.05),但左心室不良重构组梗死质量百分比[(34.07±10.04)%vs(22.20±11.29)%,P<0.001]和微血管阻塞(MVO)质量百分比[1.9(0,3.8)%vs 0(0,1.06)%,P<0.001]明显大于无左心室不良重构组。随时间推移,两组患者的心肌损伤和心功能均有恢复。但在第2次CMR时,左心室不良重构患者有更低的LVEF[(42.01±9.51)%vs(55.23±10.04)%,P<0.001]、更大的左心室收缩末期容积指数[55.58(43.15,69.91)mL/m^(2)vs 35.79(26.70,45.04)mL/m^(2),P<0.001]和梗死质量百分比[(26.71±24.51)%vs(17.08±9.25)%,P<0.001]。左心室不良重构组整体峰值应变及应变率、梗死区峰值应变、径向和周向峰值应变率更小(均P<0.05)。多因素分析显示,只有3个因素是左心室不良重构的独立预测因素,其中梗死质量百分比预测左心室不良重构的AUC为0.793(95%CI 0.693~0.873),截断值为30.67%;整体径向舒张期峰值应变率的AUC为0.645(95%CI 0.534~0.745),截断值为0.58%;肾素血管紧张素醛固酮系统(RAAS)抑制剂的AUC为0.699(95%CI 0.590~0.793)。结论在急性期,左心室不良重构组和无左心室不良重构患者的左心室容积、整体及节段的心功能没有显著差异;但随时间推移,左心室不良重构组的左心室容积明显变大,整体及节段的心功能明显更差。梗死质量百分比、径向舒张期峰值应变率及RAAS抑制剂是左心室不良重构的独立预测因子。

A rare case of isolated right ventricular non-compaction Cardiomyopathy

INTRODUCTION Isolated ventricular non-compaction is a rare congenital cardiomyopathy occurs due to arrest of normal myocardial development during embryogenesis. It is mainly diagnosed by echocar- diography through the appearance of characteristic prominent myocardial trabeculation and deep inter-trabecular spaces. Heart failore,

An unusual combination of left atrial myxoma and left ventricular non-compaction cardiomyopathy in a male patient:A Casereport

Left atrialmyxoma is a common primary cardiac tumor that is accompanied by organic heart diseases.But left atrial myxoma coexistent with left ventricular non-compaction(LVNC)is extremely rare.A young male patient with left atrial myxoma and LVNC was reported in this study.A 25-year-old manpresented to the emergency department with sudden shortness of breath and syncope,accompanied by fever and cough.He had a history ofacute ischemic strokeone year before hospitalization.Echocardiography revealed that the endocardium of the left ventricle was not smooth with raised muscle trabeculae and deep recesses.There was an oval-shaped strong echo mass with a pedicle in the left atrium attached to the atrial septum.Tumor resection was operated during extracorporeal circulation.Pathological results confirmed left atrium myxoma.In this case report,the patient had heart failure and an ischemic stroke likely of cardiogenic origin.He underwenttumor resection and started on therapeutic anticoagulation.Left atrial myxoma and LVNC are associated with poor outcomes.Early diagnosis and prompt treatment are crucial.

我国心室肌致密化不全的荟萃分析

目的了解我国心室肌致密化不全(noncompactionofventricularmyocardium,NVM)的发病现状及其临床特征、诊治方法,为临床进一步认识和诊治NVM提供依据。方法利用中国期刊全文数据库(CN-KI)、重庆维普(VIP)和万方数据库检索1989年1月～2006年6月国内报道的NVM文献81篇计300例,结合该院收治的1例共计301例病例进行分析。结果NVM可发生于任何年龄,多见于中青年。男性发病率明显高于女性。临床表现主要为进行性的心力衰竭(67.1%),其次为心律失常(9.3%)和栓塞。病变累及心脏的发生率依次为单独累及左室(82.4%)、左右室均累及(9.6%)和单独累及右室(8.0%)。35例(11.2%)合并其他先天性心脏畸形。13.9%患者具有家族遗传性。82.1%的患者曾被误诊为其他疾患,主要误诊为扩张型心肌病(69%)。经胸心脏超声检查是主要的诊断方法,但核磁共振(MRI)等检查对于部分病例同样重要。结论NVM是一种少见的未分类心肌病,有独特的病理和影像学改变,误诊率极高。应重视和充分认识其特征以提高临床诊治NVM水平。

心肌致密化不全与扩张型心肌病合并过度小梁化的对比分析

目的:探讨心肌致密化不全(NVM)与扩张型心肌病(DCM)合并过度小梁化的临床和超声心动图特点,明确对两者鉴别诊断价值。方法:对比分析31例NVM组及50例DCM合并过度小梁化组的性别、年龄、家族史、症状、心电图、脑钠肽(BNP)及超声心动图资料,着重观察两者超声心动图心腔大小、心肌壁、心内膜、彩色多普勒、血液动力学的特点,依据17节段分析法分析小梁化节段数目及程度。结果:(1)DCM合并过度小梁化组心功能分级更差,BNP明显较NVM组高(P<0.05),心脏扩大程度也更明显,差异有统计学意义;(2)NVM组患者小梁化的节段数最多,节段数(9.82±2.02)个,心尖段(第17节段)均受累,非致密化心肌厚度(NC)和致密化心肌厚度(C)比值(NC/C)大(2.84±0.61),NC/C值>2的节段数为(4.12±2.68)个;DCM合并过度小梁化组患者小梁化的节段数少,节段数(5.56±1.56)个,心尖段很少受累,NC/C值小(1.91±0.42),最多有1个节段NC/C值>2。差别均具有统计学意义(P<0.05)。结论:超声心动图是鉴别NVM与DCM的简便、实用、无创性检查手段。左心室心尖段明显呈致密化不全改变及至少2个游离壁节段收缩期的NC/C值>2可诊断NVM,并可与DCM合并过度小梁化相鉴别。

自发高血压大鼠心肌肥厚与心室颤动阈值的关系

目的探讨自发高血压大鼠心肌肥厚与心室颤动阈值的关系。方法20只雄性自发高血压大鼠,随机分成10周龄组(n=10)和18周龄组(n=10);10只10周龄雄性Wistar大鼠为对照组。分别测定3组大鼠的动脉收缩压、心脏质量指数、心室有效不应期和心室颤动阈值。结果①自发高血压大鼠的动脉收缩压和心脏质量指数明显高于Wistar大鼠(P<0.001),心室颤动阈值明显低于Wistar大鼠(P<0.001);②自发高血压大鼠中,18周龄自发高血压大鼠的动脉收缩压和心脏质量指数明显大于10周龄自发高血压大鼠(P<0.001),心室颤动阈值明显低于10周龄自发高血压大鼠(P<0.001);③不同周龄自发高血压大鼠和Wistar大鼠之间,心室有效不应期没有明显差异(P>0.05);④Wistar大鼠中心脏质量指数与动脉收缩压及心室颤动阈值均无明显相关关系,不同周龄自发高血压大鼠中,心脏质量指数与动脉收缩压及心室颤动阈值均呈明显相关关系;动脉收缩压和心脏质量指数与心室颤动阈值呈负相关(P<0.001);⑤心脏质量指数、动物周龄和种类是影响心室颤动阈值的主要因素(P<0.001)。结论肥厚心肌的心室颤动阈值降低;动脉收缩压愈高,心肌肥厚程度愈明显,心室颤动阈值愈低。

急性心肌梗死后左室重构的动态观察

目的 观察急性心肌梗死前后心肌结构的变化 ,探讨心梗后左室重构变化规律。方法 16只成年健康犬麻醉后开胸结扎前降支建立心梗模型。经胸超声心动图 (2 5MHz)分别于术前、术后 2d、术后 30d观察心脏形态、心功能及心肌应力变化。结果 术后 2d出现左室扩张 ,收缩和舒张功能减低 ,心肌应力增高 ,左房射血力增加。术后 30d较术后早期 ,左室进一步扩张 ,收缩舒张功能持续降低 ,心肌应力较术后早期高。结论 心肌梗死后早期即出现心室扩张 ,收缩和舒张功能降低 ,心肌应力增加。心梗后左室重构贯穿整个疾病过程。

心肌致密化不全患者的临床特点及预后

目的:通过分析心肌致密化不全患者的临床特点、诊断方法、治疗及预后,以提高临床诊治水平。方法:分析及随访2000年1月～2006年4月住院治疗的17例心肌致密化不全患者的临床资料、治疗及预后。结果:心肌致密化不全特征为海绵状心肌,多发生于左心室。临床表现主要为心力衰竭(纽约心功能分级Ⅱ～Ⅳ级者占88.2%)、心律失常及血栓形成(分别为88.2%与11.8%)。17例中14例为孤立性心肌致密化不全,3例合并其他心血管疾患。17例患者均行超声心动图及心脏磁共振检查,其中13例患者的超声心动图及心脏磁共振检查均明确诊断,另4例经心脏磁共振检查确诊。随访10例患者,3例行心脏移植手术,1例死亡。结论:心肌致密化不全临床表现各异,预后差。超声心动图检查是诊断主要方法,心脏磁共振检查有助于提高诊断水平。