Predictive value of local and core laboratory echocardiographic assessment of cardiac function in patients with chronic stable angina: The ACTION study.

AIMS: To evaluate the relationship between echocardiographic cardiac function and outcome in patients with stable symptomatic angina. METHODS: Baseline echo left ventricular ejection fraction and volume data measured in a central laboratory was available for 7016 patients (92% of the total) participating in the ACTION trial (A Coronary disease Trial Investigating Outcome with Nifedipine GITS). Ejection fraction was also measured by investigators. Evaluation of the different echocardiographic variables was based on adjusted hazard ratios comparing the unfavourable limit of the 90% range of the variable concerned to the favourable limit. RESULTS: The centrally measured ejection fraction was the most powerful predictor of all-cause death (adjusted hazard ratio=2.5), myocardial infarction, any stroke or transient ischaemic attack and overt heart failure (adjusted hazard ratio=4.5). The addition of either end systolic volume or end diastolic volume to ejection fraction did not materially affect the power of prediction. Compared to the central ejection fraction measurement, the investigator-measured ejection fraction was a less powerful predictor for all outcomes considered. CONCLUSION: Routine echocardiography carefully analysed by standardised methods provides useful prognostic information in patients with stable angina, including for total mortality.     

氯沙坦心衰生存研究（ELITE Ⅱ）：氯沙坦和卡托普利对心衰相关预后和症状的作用比较氯沙坦心衰生存研究（ELITE Ⅱ）：氯沙坦和卡托普利对心衰相关预后和症状的作用比较

背景：利用血管紧张素转换酶抑制剂阻断肾素-血管紧张素系统可以改善心衰（HF）患者的预后和症状。在ELITEⅡ研究中，比较了氯沙坦和卡托普利对心衰患者死亡率、发病率以及功能状态方面的作用。方法和结果：总共3152例年龄≥60岁、NYHA心功能分级为Ⅱ-Ⅳ级、射血分数≤40％的HF患者入选研究，接受氯沙坦50mg1次／d或卡托普利50mg3次／d。判断预后的指标包括：全因或HF相关的死亡、住院和停止治疗；NYHA分级的变化；生活质量（QoL）。各治疗组问HF相关预后无显著性差异。两组的NYHA分级得到了相似的改善（P〈0．01）。观察1856例患者的QoL发现，1343例患者至少存活1年以上；两组中1年存活者的QoL均得到了改善（与基线相比，P〈0．001）。     

Cardiac flow measurement by ultrafast CT: validation of continuous and pulsatile flow.

To gauge the accuracy of ultrafast CT in measuring cardiac output and myocardial perfusion in humans, measurements of continuous and pulsatile flow were made in a large asymmetrical phantom. The variation in the relationship between Hounsfield number and contrast concentration was assessed in a human thorax phantom. Radiopaque contrast medium was injected during perfusion of the phantom at a range of flow rates between 1.5 and 8 L/min. The phantom was scanned in two modes (50 and 100 ms) during continuous and pulsatile flow and with the phantom surrounded by air and by water. Flow in the tubes was calculated using indicator dilution theory, and flow in the tissue-equivalent chamber was calculated by applying first-pass distribution principles. The standard deviation of the difference between calculated and measured flow varied from 0.2 to 0.6 L/min, giving 95% limits of agreement from 0.4 to 1.2 L/min. The constant (K) relating Hounsfield unit number to iodine concentration varied widely both in different locations within the phantom and under different scan conditions (17.2-27.6 HU/mg I). Within a human thorax phantom, K varied from 14.15 to 23.18 HU/mg I and was dependent on location within the thorax phantom, the scan mode, and the cross-sectional diameter of the phantom. These data suggest that though the ultrafast CT scanner can measure continuous and pulsatile flow accurately in tubes, precise measurements of cardiac output in humans will require K to be assessed for each subject. Measurements of flow in tissue should be possible.     

Morphological and functional characteristics of myocytes isolated from human left ventricular aneurysms

Isolated single myocytes were prepared from myocardium of developing ventricular aneurysms and from myocardium within the scar of chronic ventricular aneurysms. The morphology and function of the individual cells were compared. The cells from developing aneurysms were rod-shaped, with a distinct sarcomeric structure, but did not contract even in the presence of high calcium concentrations. The sarcomere length was significantly higher than that of cells from chronic aneurysms and approached the theoretical point at which no contraction can occur. Cells from chronic aneurysms were either rod-shaped and contractile, or rounded due to hypercontracture of the myofilaments. Electron microscopy of cells from developing aneurysms confirmed the presence of elongated sarcomeres, a loss of the actin-myosin interdigitation, and damage to the contractile proteins which was particularly evident in the thin filaments. Cells with similar characteristics have also been isolated from a ruptured, ischaemic papillary muscle. These changes, which are due either to ischaemia or to overstretching of cells, may account for the weakness of the wall of developing aneurysms and be a cause of rupture or enlargement.     

Alpha-adrenoceptor stimulation, lysophosphoglycerides, and lipid peroxidation in reoxygenation induced calcium uptake in rabbit myocardium

Calcium uptake on reoxygenation of hypoxic cardiac muscle is well documented. Alpha-adrenoceptor stimulation by released catecholamines, lysophosphoglycerides and lipid peroxidation have all been suggested as mediators of this effect. We have measured the uptake of Ca2+ on reoxygenation in the isolated arterially perfused interventricular septum of the rabbit heart. The alpha agonist phenylephrine (1 mumol X litre-1) did not alter calcium uptake, and the presence of either prazosin (1 mumol X litre-1) or phentolamine (10 mumol X litre-1) did not alter the reoxygenation induced Ca2+ uptake. Lysophosphatidylcholine caused an increase in Ca2+ uptake above 8 mumol X litre-1 but also produced a simultaneous increase in the distribution volume of 51Cr-EDTA, an extracellular space marker, indicating loss of membrane integrity. Hydrogen peroxide and cumene hydroperoxide both caused an increased Ca2+ uptake, but no disruption of the cell membrane; the effect on Ca2+ uptake could be inhibited by Ni2+ ions. Alpha adrenergic stimulation and lysophosphoglycerides do not appear to be key to Ca2+ uptake on reoxygenation, but lipid peroxidation of the sarcolemma is a possible mechanism.     

The pathologic basis of Q-wave and non-Q-wave myocardial infarction: a cardiovascular magnetic resonance study

OBJECTIVES: The purpose of this study was to determine the pathologic basis of Q-wave (QW) and non-Q-wave (NQW) myocardial infarction (MI). BACKGROUND: The QW/NQW distinction remains in wide clinical use but the meaning of the difference remains controversial. We hypothesized that measurement of total MI size and transmural extent by late gadolinium enhancement cardiovascular magnetic resonance (CMR) would identify the pathologic basis of QWs. METHODS: A total of 100 consecutive patients with documented previous MI had electrocardiogram and CMR on the same day. Patients with acute MI within seven days were excluded. Left ventricular function and the size and transmural extent of MI were quantified in the three major arterial territories and correlated with the presence of QW. RESULTS: Subendocardial MI showed QW in 28%. Transmural MI showed NQW in 29%. Of all MIs, 48% were at some point transmural, and 99% of these were at some point non-transmural. As MI size and number of transmural segments increased, the probability of QW increased (anterior: total size chi-square = 53, p < 0.0001, transmural extent chi-square = 36, p < 0.0001; inferior: total size chi-square = 16, p = 0.001, transmural extent chi-square = 10, p = 0.001). These findings did not hold for lateral MI. In a multivariate model, the transmural extent of MI was not an independent predictor of QW when total size of MI was removed. The QW/NQW classification was a good test for size of MI (area under receiver operating characteristic curve: anterior 0.90, inferior 0.77). CONCLUSIONS: The QW/NQW distinction is useful, but it is determined by the total size rather than transmural extent of underlying MI.     

An experimental model of chronic cardiac failure using adriamycin in the rabbit: central haemodynamics and regional blood flow

Central haemodynamics and regional blood flow were studied comprehensively in conscious New Zealand White rabbits before and during the development of chronic low output cardiac failure produced by administration of the anticancer agent adriamycin. After eight weeks of adriamycin treatment, cardiac index fell from 326(40 to 225(56) ml.min-1.kg-1. This was accompanied by an increase in heart rate and total peripheral resistance but no change in mean systemic blood pressure. Myocardial function was shown to be depressed by the measurement of Frank-Starling curves, the slopes of which were appreciably flatter in adriamycin treated rabbits. Regional blood flow (measured by the radioactive microsphere technique) was redistributed. There were decreases in renal, splenic, small gut, and skeletal muscle blood flow, whereas myocardial and cerebral blood flow were unchanged. There was an increase in total body exchangeable sodium, indicating some salt and water retention. Systemic toxic effects of adriamycin could be limited by treating the animals for eight weeks with adriamycin and then allowing a two week recovery period before haemodynamic study. This would appear to be the optimal dosage schedule.