心肌造影负荷超声心动图研究进展

心肌造影负荷超声心动图将心肌造影与负荷超声相结合,通过检测心肌微循环完整性和心肌血流灌注情况,为临床上冠心病的评价提供了一种简便、可靠、准确的新方法。现就心肌造影负荷超声心动图研究与应用现状作一综述。     

Regional asynchrony of segmental contraction may explain the “oxygen consumption paradox” in stunned myocardium

Summary Despite apparently depressed function, stunned myocardium maintains oxygen consumption and has the capacity to increase contractility with inotropic stimulation. We hypothesized that during stunning, O₂ demand is maintained because regional segment work is performed, but is asynchronous with global left ventricular contraction, and that inotropic stimulation would restore regional work and synchrony. Thirteen open-chest anesthetized dogs were subjected to three left anterior descending (LAD) coronary artery occlusions (10 min) and reperfusions (15 min) to produce regional myocardial stunning. Segment shortening and force development were measured independently and simultaneously in the LAD (experimental) region and circumflex (control) regions. Regional myocardial work was calculated as the integrated product of instantaneous force and shortening, during two periods: 1) over the entire cardiac cycle (Positive Work), and 2) limited to the systolic portion of the cardiac cycle (Systolic Work). Regional myocardial O₂ consumption (MVO₂) was calculated from regional blood flow (radiolabeled microspheres) and O₂ saturation data (microspectrophotometry). Occlusion of the LAD produced a delay in onset of segment shortening in the ischemic region, but not in regional force development. A time delay of 67–81 ms persisted through the three stages of occlusions and reperfusion. Systolic regional work was depressed to a greater extent (924±182 to 149±118 g*mm*min^–1) than total positive regional work (1437±337 to 857±174 g*mm*min^–1). Regional subepicardial MVO₂ in the stunned region was not different than in the control region (7.3±1.5 vs. 6.9±1.4 ml O₂*min^–1*100 g^–1). Local infusion of isoproterenol reversed the delay in regional shortening from 73±7 to 21±8 ms, thereby augmenting systolic work (298%) more than positive work (60%), without a significant increase in MVO₂ (7.3±1.5 to 10.5±3.2 ml O₂*min^–1*100 g^–1). It is concluded that myocardial stunning decreases regional systolic work due to regional mechanical asynchrony, while MVO₂ is used supported total positive work which was not significantly reduced. Isoproterenol restores regional work by restoring synchrony, without greatly affecting regional MVO₂.This study was supported in part by a research grant from the Schulz Foundation and USPHS grant HL40320.     

冬眠心肌研究进展

冬眠心肌是由于冠状动脉血流减少所致的心肌及左室功能持续性损害,改善心肌灌注血流,可使心肌及左室功能异常达到部分或完全恢复。冬眠心肌存在于多种临床综合征中。冬眠心肌在血流动力学、能量物质代谢、形态和组织学特征方面均有自身的特点。临床上有多种无创性方法可用来检测冬眠心肌的存在,术前对心肌的缺血程度和范围进行准确的评估,是选择性地施行心肌血运重建术的主要依据。     

Capillary surface area is reduced and tissue thickness from capillaries to myocytes is increased in the left ventricle of streptozotocin-diabetic rats

Summary The left ventricles of normal and diabetic rats, fixed by vascular perfusion were examined using modern stereological techniques to quantify changes in the morphology accompanying streptozotocin-induced diabetes. The heart weight to body weight ratio increased in diabetic rats whilst left ventricular volume remained unchanged. Papillary muscles from the diabetic animals showed prolonged time to peak tension and relaxation, and altered sensitivity to adrenalin and calcium. The apparent cardiomyopathy observed when body weight loss exceeds heart weight loss in experimental diabetes was accompanied by specific pathological changes in the composition of the left ventricle. In the diabetic animals the volume of extracellular components increased threefold and the volume of capillaries fell. The surface density and total surface area of capillaries was reduced, and oxygen diffusion distance to myocyte mitochondria increased. The volume fraction of myocyte mitochondria was reduced during streptozotocin-induced diabetes.Abbreviations XSA cross-sectional area     

Contractile failure in early myocardial ischemia: Models and mechanisms

Summary In early myocardial ischemia we find a number of salient electrical and ionic alterations. This article reviews action potential shortening, K accumulation, and contractile failure. Enhanced K efflux during early myocardial ischemia has been attributed to a number of mechanisms, including: the inhibition of active K uptake, osmotic changes, efflux of K ions linked to anion extrusion, cation exchange, altered cellular energy levels, in particular, the opening of ATP-dependent K channels, the involvement of other ion channels, a H/K-ion exchanger, and a catecholamine-dependent pathway. The different mechanisms are discussed. Action potential shortening was described as a salient characteristic of myocardial ischemia in 1954 by Trautwein and Dudel, and was attributed to enhanced outward current. Recently it has been shown by several authors that ATP-dependent potassium channels play a key role in this context. Contractile failure in early myocardial ischemia has been explained by shortening of the action potential duration, reduced cytoplasmic free calcium levels, intracellular acidification, and a rise in inorganic phosphate and Mg. In summary, it is concluded that ATP-dependent K channels may be involved in each of these three phenomena.     

心肌细胞膜脂流动性与超微结构研究

本研究应用荧光分光光度计偏振技术研究犬实验性急性心肌梗塞早期时心肌细胞膜流动性及超微结构改变的相关程度.结果表明,冠状动脉左前降支阻断后,心肌细胞膜脂流动性明显降低,阻断前为40.952±4.623,阻断1分钟为31.936±4.008.随着缺血时间延长,,心肌细胞膜脂流动性降低越明显,阻断15和120分钟时,膜脂流动性分别为27.164±4.204和26.572±3.126(与阻断前比较,P<0.05),阻断240分钟时膜脂流动性为23.374±2.604(P<0.01,与阻断前比较).而在电镜下则见心肌组织学损坏进行性加重,因此,心肌细胞膜脂流动性的降低程度与心肌缺血时间长短和损伤程度密切相关,并与心肌组织超微结构改变相一致,是反映心肌细胞缺血损伤的一个敏感指标.     

ATP后处理对兔缺血再灌注心肌细胞凋亡及NF-κB表达的影响

目的观察三磷酸腺苷(ATP)后处理对兔缺血再灌注心肌细胞凋亡和核因子-κB(NF-κB)表达的影响。方法将64只雄性大耳白兔随机分为四组,每组16只。对照组:结扎冠状动脉前降支40 m in,再灌注180m in。缺血预处理组:3次短暂结扎冠状动脉前降支(5 m in闭塞、10 m in再灌注,重复3次),其余同对照组。缺血后处理组:方法同对照组,仅于再灌注初期结扎30 s、再灌注30 s,反复3次形成缺血后处理。ATP后处理组:方法同对照组,仅于再灌注初期自耳缘静脉泵入ATP 4 m g/kg,20 m in内滴完。应用免疫组化法测定组织中NF-κB的表达,应用TUNEL技术测定组织中细胞凋亡率,测定心肌梗死面积。结果与对照组比较,缺血预处理组、缺血后处理组和ATP后处理组细胞凋亡率明显减低,心肌梗死面积明显减小,NF-κB表达降低。结论ATP后处理对缺血再灌注损伤的心肌有保护作用,可能机制是抑制NF-κB参与的细胞凋亡。     

The effect of successful angioplasty on variables of signal-averaged electrocardiogram and ventricular wall motion in patients with a first myocardial infarction

The correlation among three variables of late potentials (LPs) obtained by signal-averaged electrocardiography (SAECG) and improvement of ventricular wall motion estimated by echocardiography were studied in 66 patients with a first acute myocardial infarction (MI). Patients with bundle-branch block, intraventricular conduction delay, multi-vessel disease, previous MI, repeat percutaneous transluminal coronary angioplasty (PTCA), or evidence of reinfarction during a 6-month follow-up were excluded. A total of 66 patients was divided into two groups, with (Group 1: n = 27, age 56 ± 11) or without (Group 2: n = 39, age 61 ± 10) improvement of ventricular wall motion. Three variables of LPs and ventricular wall motion index (WMI) estimated and scored by echocardiography at admission (WMI 1) and at 6 months after MI (WMI 2) were compared in each group. In Group 1 (WMI 1 vs. WMI 2, p < 0.002), 20 of 27 patients underwent successful angioplasty; in Group 2 (WMI 1 vs. WMI 2, p = NS), 7 of 39 patients had successful emergency angioplasty. There were significant differences in three variables of LPs between the time of admission and at 6 months after MI in Group 1 but not in Group 2. Higher incidence of LPs and greater frequency of successful emergency PTCA were found in Group 1 compared with Group 2. These results suggest that because myocardial ischemia is reversed by successful angioplasty, ventricular wall motion is improved and the arrythmogenic substrate that generates LPs is stabilized electrically. Stunned or hibernating myocardium may be the arrhythmogenic substrate that generates LPs.     

Spironolactone reduces fibrosis of dilated atria during heart failure in rats with myocardial infarction.

AIMS: Congestive heart failure (CHF) is associated with severe structural changes of atria, contributing to impaired atrial function and the risk of arrhythmia. This study investigated the effects of CHF treatments on atrial remodelling. METHODS AND RESULTS: Three months after myocardial infarction (MI), rats were treated for 1 month with spironolactone, lisinopril, or atenolol alone or in combination. Echocardiography-Doppler tissue imaging, haemodynamic measurements, and 24-h Holter monitoring were used to characterize the cardiomyopathy. Atrial fibrosis was quantified with Picrosirius Red staining. Left atrial diameter was increased (5.8+/-0.6 mm in MI vs. 3.6+/-0.3 mm in sham; P<0.0001), as was atrial fibrosis (26.7+/-3.8% in MI vs. 10.5+/-2.2% in sham; P<0.0001), which correlated with left ventricular (LV) dysfunction after 3 months of MI. P-wave duration was also increased and premature atrial beats were frequent on the 24-h electrocardiogram. Similar improvements in LV dysfunction were observed after 1 month of spironolactone, ACE-inhibitor, or beta-blocker therapy alone or in combination. Atrial hyperexcitability was reduced by all the treatments, but only spironolactone attenuated atrial fibrosis and reduced P-wave duration. CONCLUSION: Atrial fibrosis caused by chronic CHF is reduced by spironolactone.     

Apoptosis in heart failure and the senescent heart

The progressive loss of cardiac myocytes by apoptotic cell death has been discussed as an important pathogenic component in the failing myocardium as well in the aging heart. The degree to which apoptosis contributes to myocyte loss in these conditions, however, is a controversial issue. This review focuses on the regulation of apoptosis, evidence implicating apoptosis as a mechanism for the progression and development of heart failure, the role of apoptotic death in senescent cardiac dysfunction, as well as on the problems of detection of apoptosis.