Apparent Malfunction of Demand Pacemakers due to Spurious Potentials Generated by Contact Between Two Endocardial Electrodes

Malfunction of both temporary and permanent demand transvenous pacemakers was caused by contact between the two endocardial electrodes. Contact between these electrodes created spurious potentials which resulted in irregular inhibition of both demand units. The potentials were demonstrated by recording from the temporary wire. There was no interference with either pacemaker in the fixed rate mode and malfunction ceased when the temporary wire was removed.     

The Mechanism of Suppression of Proximal Tubular Reabsorption by Saline Infusions

The mechanism by which expansion of extracellular fluid volume with isotonic saline suppresses reabsorption in the proximal tubule was studied in rats by examining the relations among glomerular filtration rate (GFR), absolute and fractional reabsorption of filtrate, intrinsic reabsorptive capacity (rate of reabsorption per unit tubular volume), transit time, and tubular volume.Saline infusions reduced the per cent of the glomerular filtrate reabsorbed in the proximal tubule from 50% during antidiuresis to 25% during saline diuresis. The suppression of proximal reabsorption was the result of two factors: 1) a 30% reduction of intrinsic reabsorptive capacity, and 2) a 26% reduction of tubular volume per unit GFR.GFR invariably rose during saline diuresis. However, prevention of the rise in GFR by aortic clamping had no effect on either the inhibition of intrinsic reabsorptive capacity or the reduction in tubular volume per unit GFR produced by saline infusions. Expansion of extracellular fluid volume with isotonic saline, therefore, depressed intrinsic reabsorptive capacity and tubular volume per unit GFR by some mechanism completely independent of GFR.The effects of furosemide administration were contrasted with those of saline infusions. Furosemide inhibited intrinsic reabsorptive capacity by 40% but had no significant effect on proximal fractional reabsorption. The failure to suppress fractional reabsorption was the consequence of a disproportionate rise in tubular volume (relative to GFR) that was sufficient to completely overcome the inhibition of intrinsic reabsorptive capacity. Inhibition of intrinsic reabsorptive capacity alone, therefore, will not result in a net suppression of reabsorption of filtrate in the proximal tubule. We concluded that, although intrinsic reabsorptive capacity was inhibited during saline diuresis, the critical factor responsible for translating this inhibition into effective net suppression of proximal reabsorption was the observed reduction in tubular volume per unit GFR.     

Suppression of an External Demand Pacemaker by Diaphragmatic Myopotentials: A Sign of Electrode Perforation?

Transient pacemaker inhibition was observed in a patient with an external bipolar demand pulse generator. Recordings of the proximal, distal and bipolar electrograms showed extracardiac myopotentials only in the unipolar distal and bipolar configuration. These myopotentials which caused inhibition of the pulse generator were related to respiration and other maneuvers that resulted in active contraction of the diaphragm, thus proving their diaphragmatic origin.     

Comparison of Gold Versus Platinum Electrodes on Myocardial Lesion Size Using Radiofrequency Energy

During radiofrequency (RF) catheter ablation of arrhythmias, temperatures that approach 100°C cause a coagulum to form on the ablation electrode that results in an increase in electrical impedance and prevents further energy delivery. Since gold has nearly four times the thermal conductivity as platinum, the metal commonly used, it was postulated that gold tip electrodes could deliver more power and produce deeper lesions because of its greater heat dissipation from the electrodetissue interface to the circulating blood. To test this hypothesis, RF energy was applied to fresh bovine ventricular myocardium using 6 French catheters with 2-mm long distal electrodes made from gold or platinum. Similar studies were also conducted using 7 French catheters with 4-mm long distal electrodes. Maximum lesion depth was defined as that produced with the level of energy just below that causing an impedance rise. A maximum lesion depth of 6.2 ± 0.7 mm (mean ± SD) was obtained with the gold 2-mm electrode and 4.7 ± 0.5 mm with the platinum electrode (P = 0.003). The 4-mm gold electrode produced a maximum lesion depth of 7.2 ± 1.4 mm, while a catheter with a 4-mm platinum electrode caused a maximum lesion depth of 5.8 ± 0,7 mm (P = 0.05). We conclude that deeper lesions should be able to be made when RF energy is delivered to a gold rather than platinum tip electrode.     

心肌梗死患者健康教育需求调查分析

目的 了解不同年龄、文化程度以及不同梗死次数的患者对心肌梗死相关知识的需求情况,为制定针对性健康教育方案提供依据。方法采用自制调查问卷,对62例急性心肌梗死患者进行调查。结果 50岁以下组对病理及体力活动知识的需求程度高于50岁以上组;大专以上组对病理生理及自我保健知识的需求程度均高于中专组。结论 对患者进行健康教育时,应针对其具体需要进行。     

Permanent Cardiac Pacing with Sutureless Myocardial Electrodes: Experience in First One Hundred Patients

This report concerns our experience with a sutureless myocardial lead which we have used in 103 patients for establishment of permanent cardiac pacing. The electrode was inserted through a subxiphoid approach in all patients. Results to date indicate that this technique compares favorably with the presently popular transvenous technique as far as immediate or long-term morbidity is concerned. Complications were related entirely to pericardiotomy; no lead failure was seen during a maximum follow-up period of four years.     

One Turn More: Threshold Superiority of 3-turn versus 2-turn Screw-in Myocardial Electrodes

Epicardial electrodes are an alternative for patients in whom the transvenous approach presents technical difficulties. We have had clinical experience with two types of myocardial sutureless electrodes inserted in the anterior left ventricular wall: the 3-turn screw-in electrode (Medtronic 6917) was used in 209 patients from 1974 to 1977 and the 2-turn screw-in lead (Medtronic 6917 A) was used in 61 patients from 1978 to 1981. The initial threshold was equal and acceptable with both types of electrodes. During a follow-up period (up to 48 months), critical elevation of the pacing threshold resulting in exit block was found in 12% (25) of the patients with the 3-turn screw-in electrode and in 20% (12) of the patients with the 2-turn electrode (p less than 0.05). Elevation of the pacing threshold developed fairly early, usually within 6 months, with the 2-turn screw-in electrode, but much later, within 2-4 years, with the 3-turn electrode. During a longer follow-up time of up to 96 months the frequency of exit block increased up to 16% with the 3-turn electrode. Our results indicate that late critical elevation of the pacing threshold is surprisingly frequent with screw-in electrodes inserted into the left ventricular myocardium, and it is especially common with the 2-turn screw-in electrode.     

Fatal Infant Myocardial Infarction Caused by Ball-IN-Valve Mechanism from a Dysplastic Aortic Valve

Background

Acute myocardial infarction (AMI) can occur in infants. Early identification of AMI can allow for specific therapies aimed at improving patient outcomes.

Objective

This article describes a case of an infant with AMI caused by a previously unreported mechanism and reviews diagnostic and therapeutic strategies for dealing with this rare disease.

Case Report

We present a case of a 5-week-old infant with a fatal AMI due to a pedunculated nodule from a dysplastic aortic valve leaflet creating a ball-in-valve mechanism and occluding the left main coronary artery.

Conclusion

AMI is an important diagnostic consideration in any infant presenting with signs of unexplained cardiogenic shock. Practitioners who care for children should be aware of diagnostic and therapeutic strategies for AMI in infants.     

Suppression of a Demand Pacemaker in the Presence of Redundant Transvenous Right Ventricular Leads

A ventricular inhibited demand cardiac pacemaker was inhibited in the presence of intimate contact between the active temporary bipolar electrode ring and a retained inactive permanent bipolar electrode tip. Electromagnetic interference effects, lack of insulation, lead breaks, and loose connections were all ruled out as the cause of pacemaker suppression.     

Mechanism of Suppression of Vasopressin during Alpha-Adrenergic Stimulation with Norepinephrine

Recent studies have demonstrated that the water diuresis associated with intravenous infusion of norepinephrine is mediated primarly by suppression of antidiuretic hormone (ADH) release. To investigate whether the increase in cerebral perfusion pressure with intravenous norepinephrine (0.5 mug/kg/min) is directly responsible for suppression of ADH release, the carotid circulation of dogs was pump-perfused bilaterally to selectively increase cerebral perfusion pressure. In six experiments cerebral perfusion pressure was increased from a mean of 125 to 151 mm Hg and then returned to 120 mm Hg. This maneuver was not associated with a reversible increase in renal water excretion. The possibility was also examined that norepinephrine exerts a direct central effect to suppress ADH release. In 12 experiments norepinephrine was infused into the carotid artery in a subpressor dose (0.12 mug/kg/min) estimated to equal the amount of the catecholamine reaching the cerebral circulation with intravenous norepinephrine. The urinary osmolality (Uosm) was not significantly altered with intracarotid norepinephrine (932 to 959 mosmol/kg H(2)O. The possibility was also examined that changes in autonomic neural tone from arterial baroreceptors is responsible for suppression of ADH release with intravenous norepinephrine. In sham-operated animals intravenous norepinephrine diminished Uosm from 1,034 to 205 mosmol/kg H(2)O (P<0.001) whereas in animals with denervated arterial baroreceptors intravenous norepinephrine was not associated with a significant alteration in Uosm (1,233 to 1,232 mosmol/kg) H(2)O. These different effects on urinary osmolality occurred in the absence of differences in plasma osmolality and volume status. The results therefore indicate that norepinephrine primarily suppresses ADH release by altering autonomic baroreceptor tone rather than by a direct central or pressor effect of the catecholamine. This same mechanism may be the primary pathway for other nonosmotic influences on ADH release.     

氟尿嘧啶、伊立替康和奥沙利铂诱导小鼠心肌损伤的病理生理特征及其机制

【目的】观察氟尿嘧啶（5‐FU ）、伊立替康、奥沙利铂（OXA ）诱导心肌损伤特点并分析其可能的机制。【方法】42只昆明小鼠,分为7组,每组6只,分别给予5‐Fu、伊立替康、OXA 的最大非致死量（CMAX ）和1／2CMAX给药诱导,建立小鼠心肌损伤模型,为A1、A2、B1、B2、C1、C2组,分别腹腔连续注射上述三种药物5 d,对照组（D组）注射等量生理盐水,连续注射5d。5d后,处死小鼠,取小鼠心脏组织,HE染色检测心脏组织病理学改变;提取小鼠心肌组织蛋白,检测心肌组织中丙二醛（MDA）、过氧化氢酶（CAT）、超氧化物歧化酶（SOD）水平;Western blot法检测NF‐κB和I‐κB的表达并比较。【结果】三种化疗药物均能诱导小鼠心肌损伤,心肌间质血管周围可见出血及炎性细胞大量浸润,且CMAX损伤较1／2CMAX严重。与对照组相比,化疗药物诱导的各组MDA水平显著上升,抗氧化分子 SOD和 CAT 水平显著下降,差异均有统计学意义（ P ＜0．05）;NF‐κB在三种化疗药物诱导的心肌组织中表达上升（ P ＜0．05）,I‐κB表达下降（ P ＜0．05）。【结论】5‐Fu、伊立替康、OXA均能导致心肌组织损伤,氧化应激和NF‐κB活化可能是其主要机制。     

Mechanism of Reduced Myocardial Glucose Utilization During Acute Hypertriglyceridemia in Rats

Purpose  The purpose of the research is to study the effect of acute inhibition of intravascular lipolysis on myocardial substrate selection during hypertriglyceridemia using in vivo radiotracer analysis and positron emission tomography. Procedures  We induced acute hypertriglyceridemia in vivo using an intravenous infusion of Intralipid 20% (IL) without and with acute inhibition of fatty acid delivery from circulating triglycerides with injection of Triton WR-1339 (TRI) during a euglycemic–hyperinsulinemic clamp in Wistar rats. We determined the effect of TRI on myocardial uptake of circulating triglycerides and free fatty acids using intravenous injection of [³H]-triolein and [¹⁴C]-bromopalmitate, respectively. Myocardial blood flow, oxidative metabolism, and metabolic rate of glucose (MMRG) were determined using micro-positron emission tomography (μPET) with [¹³N]-ammonia, [¹¹C]-acetate, and 2-deoxy-2-[F-18]fluoro-d-glucose (FDG). Results  TRI reduced myocardial incorporation of [³H]-triolein but not [¹⁴C]-bromopalmitate showing that it selectively reduces myocardial fatty acid delivery from circulating triglycerides but not from free fatty acids. IL reduced myocardial blood flow and MMRG by 37% and 56%, respectively, but did not affect myocardial oxidative metabolism. TRI did not abolish the effect of IL on myocardial blood flow and MMRG. Conclusions  Hypertriglyceridemia acutely reduces myocardial blood flow and MMRG in rats, but this effect is not explained by increased myocardial fatty acid delivery through intravascular triglyceride lipolysis.     

硫化氢后处理抑制大鼠心肌损伤的机制研究

【目的】探讨硫化氢后处理对大鼠心肌缺血再灌注损伤的保护作用。【方法】健康成年S‐D雄性大鼠30只,随机分成3组,每组10只。假手术组（S组）仅开胸并分离冠状动脉左前降支,但不阻断血流150 min;缺血再灌注组（IR组）行冠状动脉左前降支阻断30 min ,再灌注120 min;硫化氢后处理组（H组）于开放左冠状动脉即刻1 min内静推硫化氢0．05 mg／kg ,再灌注120 min。再灌注末抽血测肌酸激酶同工酶（CK‐MB）水平,免疫印迹法测心肌过氧化物酶体增殖物激活受体γ（PPAR‐γ）的表达。【结果】和IR组相比,H组血清中CK‐MB的含量降低,PPAR‐γ表达增高,且两组相比较差异有显著性（ P ＜0．05）。【结论】硫化氢后处理有心肌保护作用,可能与其促进心肌PPAR‐γ表达有关。     

TLR3基因在脓毒症心肌损伤中的作用及其机制

【目的】探讨T L R3基因在脓毒症心肌损伤中的作用及其机制。【方法】选择6周雄性野生型小鼠（野生型组）和TLR3基因敲除小鼠（基因敲除组）,两组均采用盲肠结扎穿孔术（cecal ligation and puncture ,CLP）制作小鼠脓毒症模型,采用12 M Hz线阵超声探头评价两组建模前后心功能指标：心率（ HR）、左室舒／缩末期内径（LVEDD ,LVESD）,左室前／后壁舒张末厚度（ Awd ,Pwd）、左心室收缩期前、后壁厚度（ Aws ,Pws）、左室短轴缩短率（ FS％）。两组建模48 h后动脉采血及分离左心室心肌,检测小鼠血清肌钙蛋白I（cTnI）和心肌匀浆上清液中肿瘤坏死因子‐α（TNF‐α）、内皮素‐1（ET‐1）浓度。【结果】野生型组小鼠建模后心功能明显变差,表现为左室舒、缩末期内径（L V EDD ,L V ESD ）显著增大（ P ＜0．05）,FS％显著降低（ P ＜0．05）。建模后野生型组小鼠的TNF‐α和ET‐1因子在心肌浓度明显升高,且与血清cTnI 呈正相关,与 TLR3基因敲除组小鼠比较有统计学差异（ P ＜0．05）。【结论】TLR3基因是脓毒症心功能损伤的因素之一,其机制可能与炎症因子浸润心肌细胞有关。     

Myocardial infarction imaging by CT

Several recent studies have demonstrated that cardiac CT can accurately diagnose both acute and chronic areas of myocardial infarction. Furthermore, when performed in the setting of acute infarction, CT can be helpful in predicting the degree of functional recovery. Given that such findings can have important clinical implications, it is necessary to integrate the assessment of myocardial perfusion, and when available, myocardial function into the routine evaluation of contrast-enhanced cardiac CT. This article presents an overview of prior studies examining the diagnostic accuracy of detection of myocardial infarction. Building on that background, practical tips that can be helpful in the recognition of myocardial infarction are reviewed.     

Myocardial protection by volatile anesthetics

Myocardial ischaemia/reperfusion situations may occur during the perioperative period. The cardioprotective effects of anaesthetics have been known for a long time: volatile anaesthetics reduce the ischaemic cell damage and infarct development. Besides ischaemia, reperfusion itself can also lead to cellular damage, thereby further increasing the ischaemic injury (reperfusion injury). Inhalational anaesthetics offer specific protective effects against reperfusion injury in isolated hearts as well as in rabbit hearts in vivo. This protection does not depend on haemodynamic side-effects of the substances and is even present after protecting the heart against ischaemic damage using a cardioplegic solution. Short periods of ischaemia render the myocardium resistant to subsequent longer periods of ischaemia. This strongest endogenous protective mechanism against the consequences of an ischaemia is known as ischaemic preconditioning. The protective effect can also be produced by stimulation of different types of receptors: the respective agonists produce pharmacological (chemical) preconditioning. The common pathway of the signal transduction cascade of both ischaemic and chemical preconditioning includes the sarcolemnal and/or mitochondrial ATP-sensitive potassium channel. Volatile anaesthetics can imitate the protective effects of a short ischaemia, thereby producing chemical preconditioning. This effect depends, at least in part, on anaesthetic-induced opening of ATP-sensitive potassium channels.     

Suppression of interstitial nephritis by auto-anti-idiotypic immunity

Rats immunized with renal tubular antigens were protected from the development of interstitial nephritis by pretreatment with tubular antigen-reactive T lymphoblasts. Protected animals developed anti- idiotypic antibodies against idiotypes primarily within the antigen- binding region of monoclonal antitubular basement membrane antibodies. These studies extend the concept of auto-anti-idiotypic regulation to autoimmune disease, and they also provide an experimental basis for further efforts to develop biologically relevant mechanisms for attenuating the expression of other kidney diseases.