多普勒组织成像评价肥厚型心肌病左室舒张功能

目的应用多普勒组织成像脉冲技术测量二尖瓣环舒张速度,以评价肥厚型心肌病左室舒张功能.方法对90例肥厚型心肌病患者及50例正常人进行常规超声心电图及多普勒组织成像检查,测量各房室内径,室壁厚度,射血分数及二尖瓣环各点舒张早期峰值速度(Ea)、舒张晚期峰值速度(Aa).两组指标比较采用成组t检验.结果肥厚型心肌病患者室间隔厚度(25.5±6.6)mm,左室后壁厚度(9.9±2.3)mm,左室内径(42.9±5.9)mm,左房内径(39.9±4.7)mm,LVEF(71.9±4.3)%,二尖瓣血流E/A为1.42±0.7.肥厚型心肌病患者Ea较正常人减低.Aa无明显差异.结论肥厚型心肌病左室长轴主动松弛功能较正常人减低.     

Atrial fibrillation in congestive cardiomyopathy: Echocardiographic and hemodynamic correlates

Previous studies have suggested an unexpectedly low incidence of atrial fibrillation in patients with congestive cardiomyopathy. To further investigate the incidence of chronic atrial fibrillation in these patients and its relationship to left atrial dimension and pressure, we retrospectively examined M-mode echocardiographic and cardiac catheterization data from 54 patients with idiopathic (n = 29) and ischemic (n = 25) congestive cardiomyopathy. The incidence of atrial fibrillation (17%) was surprisingly low given the degree of left atrial enlargement (51 ± 5 mm; mean ± SD) and left atrial hypertension (19 ± 8 mm Hg). In addition, there were no significant differences in left atrial pressure or left atrial dimension between those congestive cardiomyopathy patients in sinus rhythm and those in atrial fibrillation, nor was there a higher incidence of secondary mitral regurgitation in patients in atrial fibrillation. Comparisons were also made between congestive cardiomyopathy patients and 21 patients with primary mitral valve disease and atrial fibrillation. Left atrial pressure was not significantly different between these groups. However, the mean left atrial dimension of the patients with mitral valve disease (56 ± 8 mm) was greater (P < 0.01) than that of patients with idiopathic (51 ± 6 mm) or ischemic (50 ± 4 mm) cardiomyopathy in sinus rhythm and also greater (P = 0.07) than left atrial dimension (51 ± 6 mm) of congestive cardiomyopathy patients in atrial fibrillation. Furthermore, massive enlargement of the left atrium (greater than 60 mm) was a common feature of mitral valve disease (33% incidence) but occurred only rarely in congestive car-diomyopathy (5% incidence). We conclude that while left atrial volume and pressure loads may be important contributors to the pathogenesis of atrial fibrillation, these factors are not sufficient to produce the arrhythmia in most patients with congestive cardiomyopathy. Other variables such as disease duration or the degree of atrial fibrosis or inflammation may also be important in determining which patients with left atrial enlargement will develop atrial fibrillation. Furthermore, massive left atrial enlargement (left atrial dimension > 60 mm) is rarely associated with ischemic or idiopathic congestive car-diomyopathy and suggests underlying primary mitral valve disease.     

Clinical and echocardiographic evaluation of the effects of atrial defibrillation in patients with idiopathic cardiomyopathy]

To elucidate the effects of atrial defibrillation in patients with idiopathic cardiomyopathy, we clinically and echocardiographically assessed 6 patients with hypertrophic cardiomyopathy (HCM) and 7 patients with dilated cardiomyopathy (DCM). Their mean age was 57 +/- 14 years and the mean duration of their atrial fibrillation (Af) was 47 +/- 29 days. There were no differences in age and the duration of Af between the HCM and DCM groups. We assessed the effects of defibrillation on the NYHA functional classification, heart rate (HR), systolic blood pressure (S-BP), M-mode echocardiographic data (LVDd, LVDs, %FS, LAD) and transmitral pulsed Doppler echocardiographic findings (peak velocity, time-velocity integral of rapid and atrial filling waves). These indices were obtained before and 52 +/- 22 days after defibrillation, and were compared with each other. 1. HR decreased (HCM: 87 +/- 16-->58 +/- 7/min, DCM: 93 +/- 19-->70 +/- 14/min) and total left ventricular filling increased (HCM: 6 +/- 1-->11 +/- 4 cm, DCM: 6 +/- 1-->10 +/- 2 cm) after defibrillation, and the increment of %FS (HCM: 36 +/- 6-->41 +/- 6%, DCM: 16 +/- 6-->25 +/- 11%) was observed. Four of 6 HCM patients and 5 of 7 DCM patients also improved with regard to the NYHA classification. 2. After defibrillation, LVDd increased in HCM (42 +/- 4-->47 +/- 4 mm), but not in DCM. However, LVDs decreased in DCM (52 +/- 9-->44 +/- 12 mm), but not in HCM. We concluded that atrial defibrillation had a beneficial effect on the recovery of the left ventricular function both in HCM and DCM due to the reduction in HR and increase in left ventricular filling. The mode of LV functional improvement after defibrillation varied depending on the state of patient's basal pathophysiology .     

Tei指数评价左心室射血分数正常的尿毒症患者的左心室功能

目的利用Tei指数评价左心室射血分数（left ventricular ejection fraction, LVEF）正常的尿毒症患者的左心功能,以了解其临床应用价值。方法选取80例LVEF正常的尿毒症患者设为尿毒症组,50名健康人设为对照组,使用Vivid7pro对两组进行检测。检测左心房内径（LAD）、左心室舒张期末内径（LVDd）、左心室收缩期末末内径（LVDs）、室间隔（IVS）及左心室后壁厚度（LVPW）、LVEF、左心室短轴缩短率（LVFS）、二尖瓣血流频谱E峰及A峰、E／A比值、左心室等容收缩时间（ICT）及等容舒张时间（IRT）、主动脉射血时间（ET）,并计算左心室Tei指数。结果尿毒症组左心房内径、左心室舒张期末内径、左心室收缩期末内径、室间隔、左心室后壁厚度均较对照组增大,差异有统计学意义（P均〈O．01）。尿毒症组的二尖瓣血流频谱E峰及A峰较对照组明显增大（P均〈0．05）、左心室等容舒张时间比对照组延长（P〈0．01）、主动脉射血时间比对照组缩短（P〈0．01）、Tei指数比对照组明显延长（0．50±0．18眠0．33±0．12,P〈0．叭）,差异有统计学意义;尿毒症组E／A比值、左心室等容收缩时间、LVEF及左心室短轴缩短率与对照组比较,差异无统计学意义（P均〉0．05）。结论测量Tei指数能比单纯LVEF更好地评价尿毒症患者的左心功能,而且方便、快捷、有效。     

Persistent left bundle branch block in a patient with dilated cardiomyopathy that improved with low dose carvedilol therapy

A 43-year-old Japanese woman with dilated cardiomyopathy had complete left ventricular bundle branch block (CLBBB), which had persisted for at least two years. At the time of admission, the serum brain natriuretic peptide (BNP) concentration was 502 pg/mL (normal range, 0-18 pg/mL), the left ventricular diastolic dimension (LVDd) was 59 mm, the left ventricular systolic dimension (LVDs) was 54 mm, the %fractional shortening (FS) was 8%, and the left ventricular ejection fraction (LVEF) was 19.7% by echocardiography. Low dose carvedilol was initiated for the treatment of heart failure. Adverse effects, such as progression of cardiac conduction disturbances, did not occur after initiation of carvedilol therapy. About one year after initiation of carvedilol therapy, the CLBBB disappeared and a significant improvement in left ventricular function was noted. The LVDd was 44 mm, the LVDs was 30 mm, the %FS was 33%, and the LVEF was 61%, and the serum BNP concentration was decreased to 18.5 pg/mL. We describe a case in which low dose carvedilol was effective for treating both CLBBB and left ventricular function.     

卡维地洛对心肌梗死后左室重塑的影响

目的：观察卡维地洛对急性心肌梗死（AMI）左室重塑的影响。方法：将80例AMI患随机分为常规治疗组（n=20)，依那普利组（n=30)及卡维地洛组（n=30)在AMI后1周，24周用超声心动图分别测定3组病人的左房内径（LA），左室舒张末期内径（LVDd)，左室收缩末期内径（LVDs)，室间膈舒张末期厚度（IVSd)，左室后壁舒张末期厚度（LVPWd)，计算左室重量（LWM），左室重量质数（LVMI）及左室射血分数（LVEF）。结果：AMI后24周，卡维地洛组和依那普利组与常规治疗组比较LA，LVDd,IVDs均明显缩小，IVSd,LVPWd,LVM及LVMI明显减小，而LVEF明显升高（P＜0．01），以上指标卡维地洛组与依那普利组比较无显性差异（P＞0．05），结论：卡维地洛可以防治AMI后左室重塑，改善心功能，其作用与依那普利相同。     

Myocardial Contraction Fraction Predicts Cardiovascular Events in Patients With Hypertrophic Cardiomyopathy and Normal Ejection Fraction

BackgroundMyocardial contraction fraction (MCF), the ratio of left ventricular stroke volume to myocardial volume, is a novel parameter that can distinguish between pathologic and physiologic hypertrophy. However, its prognostic value in hypertrophic cardiomyopathy (HCM) has never been examined. The objective was to determine if MCF is associated with functional capacity and predicts adverse cardiovascular outcomes in patients with HCM and normal left ventricular ejection fraction (LVEF).Methods and ResultsWe conducted a prospective cohort study of 137 patients with HCM and LVEF ≥55%. Patients were followed for 2.7 ± 2.5 years. We examined association of MCF with New York Heart Association (NYHA) functional class and a composite outcome of embolic stroke, heart transplantation, and cardiac death. We performed time-to-event analysis with the use of Cox proportional hazards modeling and stepwise elimination. The average age was 52 ± 18 years. The average MCF was 26 ± 11%. MCF was inversely correlated with NYHA functional class (P = .001). A total of 20 subjects experienced an outcome event with an event rate of 5.6% per patient-year. MCF independently predicted the outcome (adjusted hazard ratio 0.50 per 10% increase, 95% confidence interval 0.28–0.90, adjusted P = .02).ConclusionsIn patients with HCM and normal LVEF, MCF is associated with functional capacity and independently predicts adverse cardiovascular outcomes.     

卡维地洛对慢性心衰患者糖、脂代谢的影响

目的观察卡维地洛对慢性心衰患者的疗效及其对血糖,血脂代谢的影响。方法入选CHF患者59例,随机分为对照组:应用常规抗CHF治疗组(30例)和卡维地洛组(29例),后者在常规抗CHF治疗基础上加用卡维地洛,疗程为24周,治疗前后均测定左室舒张末期内径(LVDd)和收缩末期内径(LVDs)、左室射血分数(LVEF)、空腹血糖(FBS)、糖化血红蛋白(HbAlc)、血脂。结果卡维地洛组改善LVDd、LVDs和LVEF均优于常规抗CHF治疗组(P<0.01),治疗后卡维地络组TC、LDL-C较对照组降低(P<0.05)。结论卡维地洛可有效改善CHF患者的心功能,对糖、脂代谢有一定的益处。     

急性心肌梗死患者室壁运动及心功能损害与发病-超声检查时间的关系

目的 探索急性心肌梗死患者室壁运动及心功能损害与发病-超声检查时间的关系.方法 收集初发急性心肌梗死患者219例,均已排除陈旧性心肌梗死、早期心肌再梗死、严重的瓣膜性心脏病、先天性心脏病、心肌病等影响室壁运动及心功能的疾病.所有患者均在予冠状动脉介入干预前行经胸超声心动图检查,采用二维超声等方法测量或（和）计算左心室舒张末期内径（left ventricular diameters in diastasis,LVDd）、收缩末期内径（left ventricular diameters in systole,LVDs）、左心室射血分数（left ventricular ejection fraction,LVEF）、室壁运动计分指数（wall motion index,WMI）及运动正常节段（fragments with normal wall motion,FM）百分比等参数,并精确记录发病-超声检查时间.结果 WMI、LVDd、LVDs、LVEF、FM百分比与发病-超声检查时间的相关关系均有统计学意义（P＜0.05）,相关系数分别为0.167,0.235,0.258,-0.196,-0.144.在WMI的多重线性回归分析结果显示,变量FM百分比、LVEF、左回旋支和（或）右冠状动脉进入方程（R2=0.878,justed R2=0.876）,偏回归系数分别为-1.103,-0.030,-0.001.结论 对于未予冠状动脉介入干预的急性心肌梗死患者,其室壁运动及心功能均随发病-超声检查时间的增加而减弱.     

Characteristics of congestive heart failure accompanied by atrial fibrillation with special reference to tachycardia-induced cardiomyopathy.

BACKGROUND: Sustained tachycardia causes left ventricular (LV) systolic dysfunction leading to heart failure (HF), which is widely known as "tachycardia-induced cardiomyopathy (TIC)", but its prevalence and prognosis in Japanese remain unclear. METHODS AND RESULTS: Of 213 consecutive patients with HF associated with atrial fibrillation (AF) requiring hospitalization (n=213) between January 1999 and December 2004, and 104 (83 males, 67+/-12.6 years) were identified as not having any structural heart disease. Of them 41 (39%) had a normal LV ejection fraction (LVEF) at the initial admission, and the remaining patients fell into 2 groups: those with rapid (<6 months) normalization of the LVEF after AF management (presumed TIC, 30 patients, 29%) and those with persistent LV systolic dysfunction (dilated cardiomyopathy (DCM), 33 patients, 32%). Although the B-type natriuretic peptide value and LVEF did not differ between the 2 groups, the LV size on admission was significantly smaller in the TIC group (LV end-diastolic dimension (LVDd) 57.6+/-7.2, LV end-systolic dimension (LVDs) 49.4+/-8.0) than in the DCM group (LVDd 63.4 +/-8.8, LVDs 55.3+/-9.6, p<0.05). During a follow-up period of 42.1+/-21.2 months, cardiac death and recurrent HF hospitalization were significantly less frequent in the TIC group than in the DCM group. CONCLUSIONS: In AF-associated HF requiring hospitalization, TIC is the presumed cause in approximately one-third of patients without any previously known structural heart disease. That particular group is characterized by a relatively smaller LV and better prognosis under medical treatment.     

Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors

Idiopathic Ventricular Arrhythmias and Cardiomyopathy. Introduction: Idiopathic ventricular arrhythmias in the form of monomorphic premature ventricular contractions (PVC) and/or ventricular tachycardia (VT) can cause tachycardia‐induced cardiomyopathy (TICMP). The aim of this study was to determine the incidence, clinical and electrophysiologic characteristics, and the predictors of TICMP in patients with idiopathic ventricular arrhythmias. Methods: Study population consisted of 249 consecutive patients (148 F/101 M, 45 ± 20 y/o) with frequent PVCs and/or VT. All patients underwent transthoracic echocardiography and 24‐hour Holter monitoring. TICMP was defined as left ventricular ejection fraction (LVEF) of ≤50% in the absence of any detectable underlying heart disease and improvement of LVEF ≥15% following effective treatment of index ventricular arrhythmia. Results: Seventeen (6.8%) patients had TICMP. Patients with TICMP compared to patients with preserved LVEF were more likely to be male (65% vs 39%, P = 0.043) and asymptomatic (29% vs 9%, P = 0.018), and were more likely to have higher PVC burden (29.4 ± 9.2 vs 8.1 ± 7.4, P < 0.001), persistence of PVCs throughout the day (65% vs 22%, P = 0.001), and repetitive monomorphic VT (24% vs 0.9%, P < 0.001). PVC burden of 16% by ROC curve analysis best separated the patients with TICMP compared to patients with preserved LVEF (sensitivity 100%, specificity 87%, area under curve 0.96). Conclusions: TICMP was relatively common (～1 in every 15 patients) in our study population. The predictors of TICMP were male gender, absence of symptoms, PVC burden of ≥16%, persistence of PVCs throughout the day, and the presence of repetitive monomorphic VT . (J Cardiovasc Electrophysiol, Vol. 22, pp. 663‐668, June 2011)     

The effect of hypertension on cardiac structure and function in different types of hypertrophic cardiomyopathy: A single-center retrospective study

Objectives: To determine whether hypertension (HTN) affects cardiac structure and function in different types of hypertrophic cardiomyopathy (HCM).

Design: Patients with obstructive HCM (n = 40), septal HCM (n = 88), and apical HCM (n = 42) were separated into hypertensive and non-hypertensive subgroups, and echocardiographic parameters at baseline and at follow-up were compared between the subgroups.

Results: At follow-up, hypertensive obstructive HCM patients showed a decrease in end-diastolic volume (from 93.87 ± 26.08 mL to 79.06 ± 20.07 mL; p= 0.045) and in left ventricular end-diastolic diameter (from 45.00 ± 5.32 mm to 41.83 ± 4.58 mm; p =0.042). Non-hypertensive obstructive HCM patients showed a decrease in maximum aortic velocity (from 2.01 ± 0.53 m/s to 1.28 ± 0.25 m/s; p= 0.011) and in aortic maximum pressure gradient (from 17.22 ± 9.57 mm Hg to 6.79 ± 2.44 mm Hg; p= 0.03). Hypertensive apical HCM patients showed an increase in end-diastolic volume (from 95.28 ± 16.54 mL to 119.74 ± 25.19 mL; p= 0.016) and in left ventricular end-diastolic diameter (from 45.28 ± 3.36 mm to 50.20 ± 4.56 mm; p= 0.007).

Conclusions: HTN can affect left ventricular capacity in obstructive HCM and apical HCM, causing a decrease in ventricular capacity in the former and increase in the latter; it has no significant effect on the size of the left ventricular cavity in septal HCM. HTN can lead to a poor therapeutic effect on aortic flow rate and pressure gradient in obstructive HCM patients.     

A case of hypertrophic cardiomyopathy with progressive cavity dilatation--a review of serial 201Tl myocardial imaging

We reviewed 201Tl images of a 32 year old man with dilated hypertrophic cardiomyopathy (DHCM). At 22 years of age, when he was diagnosed as having nonobstructive hypertrophic cardiomyopathy (HCM)IVST; 20mm, Dd; 44mm, EF; 62%), 201Tl images showed only a small defect in the anteroseptal segment. At 27 years of age, when he had the first cardiac symptom as palpitation on exertion, his perfusion defect of 201Tl became wider. At 32 years age, he was hospitalized because of deterioration of congestive heart failure. Echocardiography revealed left ventricular wall thinning(IVST; 6mm), left ventricular cavity enlargement (Dd; 63mm) with a large mural thrombus and reduced left ventricular ejection fraction (EF; 32%). Thus 201Tl images may provide useful information on the process of DHCM from HCM.     

Left ventricular systolic dysfunction during exercise and dobutamine stress in patients with hypertrophic cardiomyopathy

OBJECTIVES: We sought to characterize stress-induced left ventricular systolic dysfunction in patients with hypertrophic cardiomyopathy (HCM). BACKGROUND: Myocardial ischemia and diastolic dysfunction occur in patients with HCM. We hypothesized that, in the setting of transient myocardial ischemia, left ventricular systolic dysfunction occurs during exercise and dobutamine stress. METHODS: We studied 39 patients with HCM but without obstructive symptoms at rest or coronary artery disease. A continuous ventricular function monitor equipped with cadmium telluride detectors (VEST) was used to evaluate left ventricular function during supine bicycle ergometer exercise. Dobutamine stress echocardiography (DSE) was also performed. The left ventricular ejection fraction (LVEF) and regional wall motion were determined from echocardiographic images. RESULTS: Changes in the LVEF correlated between exercise and dobutamine stress (r = 0.643, p < 0.0001). The LVEF decreased more than 5% at peak exercise in 17 of patients (group II), while the other patients had normal responses (group I). New regional wall motion abnormalities during dobutamine infusion were detected in 18 of 110 (16.4%) segments in group I and 42 of 85 (49.4%) segments in group II. Decreased or unchanged regional wall motion occurred more frequently in hypertrophied segments than in nonhypertrophied segments (p < 0.0001). There were significant inverse correlations between the LVEF responses during both stresses and the number of abnormal segments noted during dobutamine stress in all patients (VEST: p < 0.005; DSE: p < 0.0005). Signs of left ventricular obstruction were observed in 11 of 39 patients during DSE. However, there was no significant correlation between the LVEF response and the dobutamine-induced left ventricular pressure gradient. CONCLUSIONS: Exercise-induced systolic dysfunction occurred in 50% of patients with HCM. In these patients, regional wall motion abnormalities were present in hypertrophied segments.     

扩张性心肌病形成左心室血栓的相关因素分析

目的:通过超声心动图观察,探讨扩张性心肌病左心室血栓形成的相关因素。方法:根据超声心动图检查有、无左心室血栓,83例扩张性心肌病患者被分为A组(左室血栓组)和B组(左室无血栓组)。结果:左房内径、左室收缩期末内径、EF值、二尖瓣中等返流及主动脉瓣返流量在两组之间有显著差异(P<0.05~<0.01),而左室舒张末内径、室壁厚度及年龄、性别则无差异。结论:左室收缩功能的降低,左房内径的增大对左室血栓的形成有重要促进作用。而二尖瓣及主动脉瓣的中等量返流对左室血栓的形成有一定的对抗作用。     

Clinical analysis of hypertrophic cardiomyopathy which evolved into dilated phase during long-term follow-up

The aim of the present study was to analyze the incidence, clinical features and prognosis of patients with hypertrophic cardiomyopathy (HCM) which evolved into dilated phase HCM. The medical records of 43 patients with HCM followed up for at least 10 years were analyzed retrospectively. The patients were divided into two groups: group A consisting of patients with dilated-phase HCM defined by a left ventricular end diastolic dimension (LVDD) of 55 mm or more and a left ventricular ejection fraction (LVEF) of less than 50% obtained by echocardiography, and group B, consisting of patients with HCM that did not evolve into dilated phase HCM. During the mean follow-up of 16.7 years, 10 patients (23.3%) evolved into dilated phase HCM (group A) while the remaining 33 patients (76.7%) did not (group B). Ventricular tachycardia (VT) occurred in 7 of the 10 patients (70.0%) in group A and in 5 of the 33 patients (15.2%) in group B (p < 0.001). An increase in LVDD and decreases in LVEF and SV1 + RV5 in the electrocardiogram were observed during the early phase of the follow-up period in group A, while these changes were gradual in group B. Cardiac death occurred in 5 (50.0%) of the 10 patients in group A and in 2 (6.1%) of the 33 patients in group B (p < 0.001). In conclusion, dilated-phase HCM is characterized by decreases in LVEF and SV + RV5 and an increase in LVDD during the early phase of follow-up period, and is associated with an increased incidence of VT and a poor prognosis.     

原发性高血压患者左心房扩大及其影响因素

目的　分析 12 0例原发性高血压患者左心房大小及其影响因素。方法　原发性高血压患者 12 0例 ,男 5 9例 ,女 6 1例 ,年龄 33～ 78岁。全部患者分为两组 ,年龄≥ 6 0岁为老年组 (6 0例 ) ,年龄 <6 0岁为非老年组 (6 0例 )。每组根据心脏超声分为左心室肥厚和无左心室肥厚两个亚组。左心房内径大于 4cm为左心房扩大 ,面积 长度法左心室重量指数男性 >89g m2 ,女性 >77g m2 为左心室肥厚。结果　非老年组 4 3%、老年组 73%合并左心室肥厚 ;非老年组 14例 (2 3% )、老年组 2 2例 (37% )合并左心房扩大 ;37%患者左心房扩大和左心室肥厚同时并存 ,2 0 %患者仅有左心房扩大 ;两组左心房扩大者共 36例 ,其中老年组合并左心室肥厚占 5 0 % (18 36 ) ,非老年组合并左心室肥厚占 2 2 % (8 36 ) ;多因素分析提示超重、血压水平与左心房扩大无显著相关性 ,年龄和左心室重量指数同左心房扩大显著相关。结论　年龄与左心室肥厚是原发性高血压左心房扩大的重要影响因素。     

老年左心室功能不全患者行冠状动脉内支架术

目的　评价左心室功能不全对老年冠心病患者选择性冠状动脉内支架术安全性和远期预后的影响。方法　4 76例老年冠心病患者行选择性冠状动脉内支架术 ,其中 73例左心室射血分数 <4 0 % (左心室功能不全组 ) ,4 0 3例左心室射血分数≥ 4 0 % (对照组 )。分析两组患者手术结果和远期预后。结果　两组支架术成功率 (95 .8%和95 .9% )和手术并发症相似 (2 .2 %和 2 .7% ,P >0 .0 5 )。在 (16± 8.4 )个月随访期中 ,左心室功能不全组死亡率较对照组显著增高 (14 .1%和 3.2 % ,P =0 .0 0 1)。多因素分析显示 ,左心室射血分数是老年患者冠状动脉内支架术后远期死亡的独立预测因素 (RR 0 .95 0 ,95 %CI0 .919～ 0 .981,P =0 .0 0 2 )。结论　左心室功能不全的老年冠心病患者选择性冠状动脉内支架术安全 ,但远期死亡风险较高     

Left ventricular diastolic filling in patients with left ventricular dysfunction

The pattern of abnormal left ventricular diastolic filling and its specificity in coronary disease patients with severe left ventricular dysfunction has received little attention. We evaluated the left ventricular diastolic filling curve derived from gated blood pool scans in 21 normals, 61 coronary disease patients with ejection fractions less than or equal to 30%, and 51 congestive cardiomyopathy patients with ejection fraction less than or equal to 30%. The peak filling rate (PFR), peak ejection rate (PER), PFR/PER and the % stroke volume filled at 1/3 of diastole (%SV-1/3 DT) and at the end of the rapid filling period (%SV-RFP) were determined for each group. The PFR and PER were reduced in both coronary disease and congestive cardiomyopathy groups. The PFR/PER was increased in the coronary disease group (1.19 +/- 0.28) and congestive cardiomyopathy group (1.21 +/- 0.32) as compared to normals (0.93 +/- 0.20, P less than 0.001). A greater %SV-1/3 DT and %SV-RFP were noted in both coronary disease and congestive cardiomyopathy groups. Coronary disease and congestive cardiomyopathy patients with a mean pulmonary capillary pressure (PCP) greater than or equal to 18 mm Hg had a greater PFR/PER, %SV-1/3 DT, and %SV-RFP than patients with a PCP less than 18 mm Hg. An abnormal and nonspecific pattern of left ventricular diastolic filling is present in both coronary disease and congestive cardiomyopathy patients and is characterized by an increased PFR/PER, a greater %SV-1/3 DT, and a greater %SV-RFP. This pattern may be related to elevated PCPs.     

Characteristics of premature ventricular complexes as correlates of reduced left ventricular systolic function: study of the burden, duration, coupling interval, morphology and site of origin of PVCs

PVCs and Left Ventricular Dysfunction. Background: Frequent premature ventricular complexes (PVCs) can cause a decline in left ventricular ejection fraction (LVEF). We investigated whether the site of origin and other PVC characteristics are associated with LVEF. Methods: We retrospectively studied 70 consecutive patients (mean age 42 ± 17 years, 40 [57%] female) with no other cause of cardiomyopathy undergoing ablation of PVCs. We analyzed the association of a reduced LVEF, defined by LVEF <50% on echocardiography, with features of PVCs obtained from electrocardiography, 24‐ or 48‐hour Holter monitor and electrophysiology study. Results: Patients with reduced LVEF (n = 17) as compared to normal LVEF (n = 53) had an increased burden of PVCs (29.3 ± 14.6% vs 16.7 ± 13.7%, P = 0.004), higher prevalence of nonsustained ventricular tachycardia (VT) [13 (76%) vs 21 (40%), P = 0.01], longer PVC duration (154.3 ± 22.9 vs 145.6 ± 20.8 ms, P = 0.03) and higher prevalence of multiform PVCs [15 (88%) vs 31 (58%), P = 0.04]. There was no significant difference in prevalence of sustained VT, QRS duration of normally conducted complexes, PVC coupling interval, or delay in PVC intrinsicoid deflection. Patients with fascicular PVCs (n = 5) had higher mean LVEF compared to others (66.2 ± 4.0% vs 53.0 ± 10.0%, P = 0.002). There was no association of LVEF with other PVC foci or with left‐bundle versus right‐bundle branch block morphologies. The threshold burden of PVCs associated with reduced LVEF was lower for right as compared to left ventricular PVCs. Conclusion: In addition to the PVC burden, other characteristics like a longer PVC duration, presence of nonsustained VT, multiform PVCs and right ventricular PVCs might be associated with cardiomyopathy. (J Cardiovasc Electrophysiol, Vol. 22, pp. 791‐798, July 2011)