Left bundle branch block: prevalence, incidence, follow-up and outcome

In a randomly selected population screening study of 8450 menand 9039 women 33 to 71 years of age conducted in Iceland in1967–1977, 27 men and 17 women were found to have leftbundle branch bock (LBBB). The prevalence of LBBB at that timewas 0.43% for men and 0.28% for women. The incidence of LBBBwas 3.2 per 10 000 per year for men and 3.7 per 10 000 per yearfor women.All except one of 37 alive patients with LBBB wereexamined in 1984 including chest X-ray, echocardiography andexercise testing (Bruce protocol). Eight men had had myocardialinfarction (P<0.05), 12 had angina pectoris, 15 had hypertension,7 had cardiomyopathy, 13 had primary conduction disease, and3 had pacemakers. Five men and two women had died in comparisonwith 18 men and 1 woman in an age-matched control group of 176people (P ns). Three of 5 decreased LBBB men had cardiomyopathyat autopsy. Three men died suddenly. The two women died of noncardiaccauses. Only one patient in the control group had cardiomyopathy(P< 0.01). There was no significant difference in other cardiacdiagnoses between the groups. Eleven LBBB women out of thirteenhad a normal exercise duration (6 min) and 11/17 men exercisednormally (7 min). In comparison with the control group, theLBBB patients had an increased LV diameter 2.85±0.38vs 2.58±0.38 cm m^-2 body surface area (P<0.01). Therewas no difference between the groups in left atrial diameteror LV wall thickness.In conclusion, the prevalence of LBBB was0.43% for men and 0.28% for women of middle age. The incidencewas 3.2 per 10 000 per year for men and 3.7 per 10 000 per yearfor women. The prognosis of LBBB is relatively benign apartfrom its association with dilated cardiomyopathy. Few patientsrequire pacemakers. The mean LV diameter is increased in randomlyselected patients with LBBB, but only those with an underlyingdisorder.     

Substantia nigra damage induced by ischemia in hyperglycemic rats

Summary Preischemic hyperglycemia induced by feeding or glucose infusion worsens the brain damage and the clinical outcome following ischemia of a given duration and density, and characteristically causes postischemic seizure activity. Light microscopy has previously showed that, in the rat, transient hyperglycemic ischemia induced by bilateral carotid occlusion in combination with arterial hypotension causes a uni- or bilateral lesion in the pars reticulata of the substantia nigra. Since this region has a central role in preventing seizure discharges the present study was carried out to determine the ultrastructural characteristics of this lesion. In rats with 10 min of transient hyperglycemic ischemia followed by recirculation for 1 to 18 h, the pars reticulata of the substantia nigra showed signs of status spongiosus, as well as extensive nerve cell alterations. These changes were observed after all recovery periods studied. The spongiotic appearance was mainly caused by swelling of dendrites and, to a lesser degree, by astrocytic swelling. The dendrites were expanded at all recovery times but the severity increased during the later periods of recirculation. These swollen dendrites contained severely expanded mitochondrias and endoplasmic reticulum. The cytoskeletal elements showed disordered lining of microtubules. Two major types of nerve cell alterations were present: a pale and a dark variety. The pale type was the most frequent cell alteration. It occurred in all experimental groups and at all time points. Redistribution of the nuclear chromatin and of cytoplasmic organelles as well as swelling of the same type as in the dendrites were the essential changes. The dark neurons were much fewer in number and occupied a peripheral position in the pars reticulata. Astrocytic foot processes appeared to be dilated around the dark neurons. Swelling of astrocyte processes was most pronounced in the 1 h recovery animals. Both types of neurons showed severe mitochondrial alterations of the type observed in dendrites. Occasionally, mitochondrial alterations were found in astrocytic processes as well. Blood vessel alterations were lacking. Previous studies have shown that in this model of ischemia the substantia nigra has a relatively well-preserved blood perfusion. In view of this the extensive histopathological lesions are surprising. We speculate that the lesions primarily involve excitotoxic damage to dendrites, with pronounced lactic acidosis playing a contributory role in causing axonal and glial pathology as well.Supported by grants from the Swedish Medical Research Council (project 12X-03020 and project 14X-263) and from the U.S. Public Health Service via the N.I.H. (grant No. 5 RO1 NS07838)     

Repeated short periods of regional myocardial ischemia: effect on local function and high energy phosphate levels

Summary The effect of recurrent periods of ischemia on the myocardium was investigated in 15 open-chest dogs. Ischemia was produced by 3 minutes of proximal occlusion of the left anterior descending coronary artery. Each occlusion was followed by reperfusion of 3 minutes duration. Forty occlusions with a total of 120 minutes of ischemia were performed, and regional function (sonomicrometry) as well as high energy phosphates (needle biopsies) were determined at the end of the 5th, 20th, and 40th period of ischemia and reperfusion. The first periods of ischemia had a cumulative effect both on regional postischemic function (44% and 59% respectively of preischemic control after 20 occlusions) and on the ATP content, but with increasing number of occlusions the additive effects became smaller (ATP reduction/mol/gww/per occlusion). The ATP breakdown per occlusion was diminished with increasing number of periods of ischemia, and no significant adenosine was measured in the ischemic myocardium. Higher than normal postischemic creatine phosphate levels (9.1 mol/g w w at the 40th reperfusion vs. 6.7 mol/gw w control) indicated a functioning oxidative phosphorylation in the presence of an ATP utilization problem at the sarcomere level, because indicators of the cellular energy level (energy charge, free energy change of ATP hydrolysis) quickly normalized during reperfusion. Stunned myocardium is therefore not a problem of energy supply but rather of energy utilization. Reduced ATP utilization and regional dysfunction are the expressions of the same cellular defect which resides either in the ATP-splitting contractile apparatus or in the electromechanical coupling. Contractile dysfunction during reperfusion protects the heart against subsequent periods of ischemia because ATP turnover is reduced.Parts of the results were presented at the 57th Sessions of the American Heart Association, Miami, Florida/U.S.A. 1984     

Regional cerebral blood flow after occlusion of the middle cerebral artery

Occlusions of the middle cerebral artery (MCA) are mostly of embolic origin (appr. 80%) and give rise to about one third of all ischemic strokes, most of these being major strokes. MCA occlusions lasting for less than 1/2 h are tolerated without occurrence of permanent tissue damage. Occlusions lasting between 1/2 h to 4-8 h lead to permanent tissue damage and neurological deficits that are proportional to the duration of occlusion. Maximal tissue damage is obtained after 4-8 h occlusion. A cerebral blood flow of 8-23 ml/100 gr/min is sufficient for cellular viability but insufficient for normal tissue function ("ischemic penumbra"). Cellular function is completely abolished in the interval 8-16 ml/100 gr/min and flow at that level is tolerated only for 1-3 h before neuronal death ensues. In the interval 18-23 ml/100 gr/min there is some functional activity although it is reduced. Experimental and clinical evidence suggests that flow in this interval may be tolerated for several days, months or even longer ("chronic ischemic penumbra"). After MCA occlusion the blood flow falls below 8 ml/100 gr/min in most cases and permanent MCA occlusion always leads to relatively large areas of frank infarction. The ischemic infarcts may be surrounded by collaterally perfused areas where the blood flow is pressure-dependent (impaired autoregulation) and quite commonly insufficient for normal neuronal function (below 23 ml/100 gr/min). Such collaterally perfused areas may include a "chronic ischemic penumbra". Emboli causing MCA occlusions commonly disintegrate and/or migrate more peripherally within the first few weeks post stroke. This leads to reperfusion and changes of ischemic infarcts into hyperemic infarcts where flow is severely increased. The vascular reactivity is completely abolished in hyperemic infarcts and the hyperemic state lasts for about two weeks. Probably, anemic infarcts are equivalent to ischemic infarcts while the hemorrhagic variety is equivalent to hyperemic infarcts. The "partial infarct" with selective neuronal necrosis occurs in experimental animals after MCA occlusions of less than four h but not after permanent MCA occlusion. The significance of partial infarction in human stroke is not clarified. The extent of irreversible tissue damage can be reduced only if therapy sets in within 4-8 h after the occlusion. If a "chronic penumbra" exists the extension of reversible tissue damage can be reduced if therapy aimed at increasing the blood flow in the penumbra sets in within weeks or even months after the stroke.(ABSTRACT TRUNCATED AT 400 WORDS)     

Heparin inhibition of polymorphonuclear leukocyte activation in vitro. A possible pharmacological approach to granulocyte-mediated vascular damage

The "in vitro" effects of heparin on different functions of human polymorphonuclear leukocytes were studied. Granulocyte aggregation, enzyme release induced by FMLP and zymosan-activated serum and superoxide anion and chemiluminescence generated by FMLP were assessed. Heparin (25-500 micrograms/ml) was able to inhibit in a dose-dependent way cellular aggregation and degranulation induced either by FMLP or by zymosan-activated serum. FMLP-dependent superoxide anion generation and chemiluminescence were specifically inhibited by heparin at the concentration of 25 micrograms/ml. Our results showed that heparin "in vitro" inhibits all the aspects of the functional and metabolic granulocyte activation. A possible protecting effect of the drug on leukocyte-mediated tissue injury and vascular damage is discussed.     

Assessing the Impact of Salt Reduction Initiatives on the Chronic Disease Burden of Singapore

Globally, many countries are facing an increasing burden of chronic disease due to ageing populations, of which cardiovascular disease forms a large proportion. Excess dietary sodium contributes to cardiovascular disease risk and requires intervention at a population level. This study aimed to quantify the impact of several salt reduction initiatives on population health over a 30-year horizon using GeoDEMOS, a population model from Singapore. Four interventions were modelled in four demographic groups in 2020 for a total of 16 intervention scenarios. The effect of 0.5, 2.0, and 4.0 g/day reductions in daily salt consumption, along with adherence to the World Health Organization guidelines of a maximum of 5.0 g of salt each day, was modelled in the entire population, including the overweight and obese, the elderly, and diabetics. In each scenario, the number of averted incident cases of acute myocardial infarction and stroke, along with the disability-adjusted life years up to 2050, was monitored. We found 4.0 g/day reductions in salt consumption were the most effective when implemented across the entire population, resulting in 24,000 averted incident cases of cardiovascular disease and 215,000 disability-adjusted life years over 30 years. This is a large figure when compared with the 29,200 projected annual incident cases of cardiovascular disease in 2050. When targeted at specific high-risk demographic groups, the largest effects were observed in the overweight and obese, with the same intervention yielding 10,500 averted incident cases of cardiovascular disease and 91,500 disability-adjusted life years. Quantifying the benefits of salt reduction initiatives revealed a significant impact when administered across the entire population or the overweight and obese. Health promotion efforts directed toward sustainably reducing salt consumption will help to lower the chronic disease burden on the healthcare system in years to come.     

急性心肌梗塞Q－T离散度分析－－附68例临床报告

目的：探讨急性心肌梗塞（AMI）患首次心电图Q－T离散度（Q－Td)及Q－Tc离散度（Q－Tcd）与严重室性心律失常发生的关系,对预后进行评估。方法：对68例AMI患首次心电图Q－Td及Q－Tcd进行测定。结果：18例AMI并室速室颤组患Q－Td,Q－Tcd显高于50例非室速室颤组患;结论：AMI患Q－Td及Q－Tcd值增大,室速室颤发生率增加,两呈正相关关系,易发生心源性猝死。故Q－Td及Q－Tcd可作为AMI病情危重预后差的标志,对判断预后有重要临床意义。     

中华眼镜蛇毒F组分对沙鼠脑缺血再灌注损伤的保护作用

目的：研究中华眼镜它毒F组分脑缺血再灌注损伤的保护作用,方法：结扎沙鼠双侧颈总动脉1h,造成前脑缺血模型,用比色法测定脑匀浆过氧化脂质的最终产物丙二醛（MDA）的含量及超氧化物歧化酶（SOD）的活性,结果：F组分0．9,0．3,0．1mg/kg可显著抑制脑内脂质过氧化,降低MDA的含量,并提高超化物歧化酶的活,性且呈一定的量效关系,同缺血再灌组比较P＜0．05,同阳性对照药尼莫通比较,P＞0．05,结论：中华眼镜蛇毒F组分对脑缺血再灌注损伤有保护作用,可能与抑制自由基的生成和促进自由基的清除有关。     

自发性高血压大鼠左室不同部位心肌纤维化程度的改变: 病理变化与心肌密度改变的对比观察

目的：探讨自发性高血压大鼠（SHR）左室室间隔、前壁、后壁及侧壁 心肌纤维化的动态变化,以及心脏超声显像结合计算机分析检测心肌密度这一方法的可靠性。方法：应用病理及生化检查,检测SHR左室室间隔、间壁、后壁及侧壁心肌纤维化的病变程度;通过心脏超声显像并结合计算机分析,检测大鼠的心肌密度的变化。结果：14周时,代表心肌纤维化水平的参数羟脯氨酸浓度（HC）在SHR室间隔、前壁及后壁即已增高,以室间隔最为明显,而左室侧壁虽有增高趋势,但未达到显著性水平;24周时各部位均明显增加,但各部位之间的差异明显减少。在14周时,代表血管周围纤维化水平的参数血管周围胶原面积（PVCA）在左室各部位较对照组均显著增高,24周时增高更为明显,但各部位之间无显著性差异。而代表间质纤维化水平的参数胶原容积分数（CVF）在14周时只有室间隔显著增高,其余各部位无明显变化;24周时各部位均有显著增高,但仍以室间隔增高最为明显。心肌灰度均值在14周时各部位均较对照组显著增高,各部位之间比较,室间隔最高,侧壁最低,二者之间有显著性差别。24周时各部位均较14周显著增高,但各部位之间差别变小。在室间隔,灰度离散度在14及24周均未出现显著性改变,而其他部位则在14周时增高,24周时趋于正常。结论：在高血压发病过程中,心肌纤维化尤其是间质纤维化的变化程度是不均衡的,以室间隔程度最重,左室侧壁最轻;应用心脏超声显像并结合计算机分析测定心肌密度,可客观地反应心肌纤维化的程度。     

蜕皮甾酮对冠状动脉闭塞致大鼠心肌梗死的有益作用及机制

目的 探讨植物有效成分蜕皮甾酮（ecdysteron,EDS)对心肌梗死有益作用,并探讨其机制。方法 采用冠状动脉左前降支结扎致大鼠心肌梗死模型,ip EDS,连续7d。测定血清肌酸磷酸激酶（CPK）、谷草转氨酶（GOT）、乳酸脱氢酶（LDH）活性、心肌梗死面积、冠状动脉血清、毛细血管密度及血管内皮生长因子（VEGF）的表达量。结果 0．5,5,50mg/kgEDS能剂量能依赖地影响大鼠血清CPK、GOT、LDH活性,以5mg/kg剂量的EDS降低心肌酶谱为最佳。5mg/kgEDS能明显减少心肌梗死面积、增加冠状动脉血流量、毛细血管密度和VEGF表达量。结论 EDS能减轻冠状动脉结扎致心肌梗死,机制在于促进VEGF的表达和毛细血管再生及增加冠状动脉血流量。