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ObjectiveWe characterised the clinical course, treatment and outcomes in 59 patients with relapsing myelin oligodendrocyte glycoprotein (MOG) antibody-associated demyelination.MethodsWe evaluated clinical phenotypes, annualised relapse rates (ARR) prior and on immunotherapy and Expanded Disability Status Scale (EDSS), in 218 demyelinating episodes from 33 paediatric and 26 adult patients.ResultsThe most common initial presentation in the cohort was optic neuritis (ON) in 54% (bilateral (BON) 32%, unilateral (UON) 22%), followed by acute disseminated encephalomyelitis (ADEM) (20%), which occurred exclusively in children. ON was the dominant phenotype (UON 35%, BON 19%) of all clinical episodes. 109/226 (48%) MRIs had no brain lesions. Patients were steroid responsive, but 70% of episodes treated with oral prednisone relapsed, particularly at doses ConclusionRelapsing MOG antibody-associated demyelination is strongly associated with ON across all age groups and ADEM in children. Patients are highly responsive to steroids, but vulnerable to relapse on steroid reduction and cessation.

In the ECG of a diabetic patient without coronary artery disease, a double T wave was observed. The ECG was normal the next day. This finding was interpreted as representing repolarization abnormalities (e. g., myocardial ischemia) by many health care workers. However, it represents an artifact called "pseudo double T wave". The cause is unknown but most likely due to abnormalities at the interface between surface electrodes and skin tissue. The diagnosis of ECG artifacts requires meticulous examination of the tracings coupled with a thorough knowledge of normal patterns.

Objective Abnormalities in circulating ghrelin have been reported in chronic liver disease. This study assessed the response of anabolic peptides ghrelin, growth hormone (GH) and insulin-like growth factor 1 (IGF-1) in patients with alcoholic cirrhosis and healthy subjects to oral glucose. In a previous study, using oral glucose we identified loss of ghrelin regulation in nonalcoholic steato-hepatitis. Patients/Design/Measurements Fourteen patients with alcoholic cirrhosis were compared with 11 healthy subjects. Patients with cirrhosis were studied when adjudged clinically stable in hospital. After an overnight fast, they ingested 100-g glucose dissolved in 250 ml of water. Blood was sampled before and every 20 minutes after ingestion for 120 minutes. Plasma acylated and des-acyl ghrelin, GH, IGF-1 and insulin were assayed by ELISA. Results Expressed as median (95% CI): 120-minutes integrated acylated ghrelin was 26 (19-66) in controls compared to 170 (129-252) pg/ml per hour in patients with cirrhosis; P < 0 center dot 001. Both groups exhibited a normal postglucose plasma total ghrelin profile. Among patients with cirrhosis (compared to controls), growth hormone was increased 15-fold and IGF-1 decreased 4-fold. Acylated ghrelin correlated with GH (Spearman r = 0 center dot 69, P = 0 center dot 0015) in control subjects but not in patients with cirrhosis. Conclusions Acylated ghrelin is markedly increased in alcoholic cirrhosis, with apparent preservation of normal postprandial mechanisms of gastric ghrelin secretion. GH is also increased; however, its correlation with acylated ghrelin (confirmed in healthy subjects) is absent in patients with cirrhosis. Despite increased ghrelin and GH, patients with alcoholic cirrhosis remain anorexic and catabolic suggesting potential tissue resistance to the actions of these anabolic peptides.

To evaluate the applicability of myocardial contrast echocardiography for the assessment of coronary blood flow reserve, 21 consecutive patients undergoing coronary angiography were studied. Only patients with a single left anterior descending lesion or normal coronary angiogram were included. Intracoronary injections of sonicated albumin were performed before and after the administration of intracoronary papaverine. Good quality studies at baseline and after the administration of papaverine were obtained in 14 of 21 patients. Ten patients had a significant (greater than 75%) single left anterior descending lesion and four had normal or insignificant lesions (70% or less stenosis) in the left anterior descending coronary artery. Time-intensity curves for the left anterior descending coronary artery region of interest were generated and then the peak contrast intensity (PCI), washout half-time (T1/2) and the area under the curve (AUC) were calculated. The post-papaverine increases in PCI and in the AUC, compared to baseline, were 55 +/- 22% and 102 +/- 14% in the four patients with 70% or less left anterior descending diameter stenosis serving as a control group and 3 +/- 25% and 40 +/- 10%, respectively, in the 10 patients with significant left anterior descending coronary artery disease (mean +/- 1 SD, P less than 0.01). In patients with normal coronary arteriography T1/2 increased after intracoronary injection of papaverine. In patients with severe lesions, either an increase or a decrease in T1/2 was observed. Significant left anterior descending coronary artery stenosis associated with impaired coronary blood flow reserve can be detected by failure of myocardial contrast echocardiographic parameters to increase after injection of papaverine. Mild and transient side effects were noted in three patients.

POSSUM and its variants Portsmouth POSSUM (P-POSSUM) and Colorectal POSSUM (CR-POSSUM) equations were derived from a heterogeneous general surgical population, which have been used successfully to provide risk-adjusted operative mortality rates. CR-POSSUM utilises fewer parameters, allowing ease of use. The aim of this study was to predict the mortality outcome in colorectal surgery using these scoring systems compared to the observed mortality and to devise a new scoring system with improved accuracy. The study was conducted prospectively on all consecutive patients requiring elective and emergency colorectal surgery between April 2002 and May 2005. The outcome parameter was defined as 30-day mortality. The observed mortality was compared with predicted mortality by the scoring systems. Hosmer and Lemeshow test was used to assess statistical accuracy of POSSUM. Eight hundred ninety-nine patients underwent colorectal surgery during the study period. There were 619 elective and 281 emergency patients. Observed 30-day mortality rate was 9%, compared with predicted mortality rate of 13.5% with POSSUM, 5% with P-POSSUM and 9.5% with CR-POSSUM. POSSUM’s mortality rate was overestimated, while P-POSSUM’s mortality rate was underestimated. CR-POSSUM, the simplest system of all three, most accurately predicted mortality in our unit.

Crohn’s disease is a chronic non-specific, transmural inflammation of the gastrointestinal tract of unknown aetiology. It may affect any part of the gastrointestinal tract from the mouth to the anus and may be associated with extraintestinal manifestations. In the gastrointestinal tract, involvement of the ileum is the most common pattern of presentation. The disease commonly affects people between 15 and 30 years of age. Both sexes are equally affected. The disease affects urban dwellers more than rural dwellers and is associated with higher socio-economic class.

Significant numbers of infiltrating mononuclear cells are commonly observed in solid tumours, although their role in restricting tumour growth is not clear. Tumour-infiltrating lymphocytes (TIL) from 38 patients with colorectal cancer, in parallel with peripheral blood lymphocytes (PBL), were assayed to determine their ability to proliferate in response to concanavalin A (ConA), interleukin-2 (IL-2), ConA+IL-2, phorbol 12-myristate 13-acetate (PMA)+ionomycin ionomycin (IOM), and staphylococcal enterotoxin B(SEB). These reagents were selected to give a range of weak to strong proliferative responses either via or independent of the T cell receptor. Proliferation of TIL was significantly lower than that of PBL in all cultures: ConA (P0.001), IL-2 (P = 0.002), ConA+IL-2 (P0.001), PMA+IOM (P0.001), SEB (P = 0.002). In addition to the low proliferative capacity of TIL, production of cytokines by TIL may also play a role in control of tumour growth. We have assayed IFN gamma production in the supernatants from 16 paired TIL and PBL cultures, and tumour necrosis factor alpha (TNF alpha) in 6 paired cultures. TNF alpha concentrations were significantly lower in TIL cultures than in PBL cultures stimulated with ConA (P0.05), but no different in control or IL-2 stimulated cultures. IFN gamma levels did not significantly differ between PBL and TIL cultures, indicating that despite the restricted proliferative capacity of TIL, these cells remain capable of secreting significant amounts of IFN gamma.

A 50-year-old woman with Beçhet's disease presented with episodic diarrhoea and generalised abdominal pain. She was on regular mycophenolate maintenance therapy, being intolerant of both ciclosporin and azathioprine. Previous rectal biopsy was consistent with colitis, probably associated with Beçhet's disease. During this admission, she began passing faecal matter per vaginam. Digital rectal examination confirmed the presence of a large rectovaginal fistula. She underwent urgent laparotomy for a subtotal colectomy with end ileostomy. Although there were no signs of septicaemia preoperatively, small perforations were identified in the caecum and at the splenic flexure on laparotomy. Histopathology confirmed the presence of multiple shallow ulcers throughout the colon with features suggestive of Beçhet's colitis.

This report describes reprogramming of a pulse generator consequent to cardiac defibrillation. Analysis of the explanted pulse generator revealed normal function. We tested the electrical properties of several defibrillators and our studies suggest that erratic electrostatic discharges at the time of paddle application before defibrillation may create a signal sequence capable of reprogramming the particular pulse generator by activating either the reed switch or internal electronics.

This report describes the clinical course of a patient with bradycardia and tachycardia-dependent atrioventricular block. Bradycardia dependent A-V block (phase 4 block) was transient and precipitated by spontaneous slowing of the sinus rate, atrial and ventricular extrasystoles; The degree of slowing (critical RP interval) required to induce A-V block increased progressively over a three-day period. Bradycardia-dependent A-V block was terminated mostly by critically times spontaneous or paced ventricular escape beats, but normally conducted atrial impulses also appeared to restore A-V conduction on several occasions. The tachycardia-dependent component was manifested by an unusual fatigue phenomenon in the His-Purkinje system seen only at an atrial pacing rate of 150 per minute. These observations document the presence of both bradycardia and tachycardia-dependent A-V block in the presence of a normal H-V time and also illustrate the dynamic nature of both phase 4 block and the period of "supernormal" intraventricular conduction.

It is well known that removal of a testing magnet from a DDD pulse generator may cause endless loop tachycardia in patients with retrograde ventriculoatrial conduction; application of the magnet then terminates the tachycardia. We have observed the opposite response to the magnet and in this report we describe the paradoxical induction of endless loop tachycardia by magnet application over a DDD pulse generator and its persistence despite repeated removal and reapplication of the magnet. This unusual behavior occurred only in the "magnet off" function and is due to magnet-induced signals sensed by the atrial channel circuitry.

This report describes familial cardiac myxoma involving parent and child. The familial occurrence of this condition, previously reported in four other families, underscores the necessity of screening all direct members of the family by echocardiography once the diagnosis of cardiac myxoma is made. Each patient presented with unusual clinical manifestations. The father, who had a right atrial myxoma associated with an atrial septal defect and mitral valve prolapse, presented with findings highly suggestive of paradoxical embolism. The daughter, who had an infected right ventricular myxoma, was initially treated for valvular subacute bacterial endocarditis before the diagnosis was made.

Signals responsible for pacemaker oversensing may arise from the pacing system itself, P or T wave, concealed ventricular extrasystoles, skeletal muscle potentials, and distant electromagnetic fields. Oversensing is the most common cause of pacemaker pauses and a common clinical problem during follow-up of patients with implanted pulse generators. This article reviews the mechanisms and diagnosis of oversensing and the importance of multiprogrammability for its treatment.

Transient Q waves in the absence of myocardial infarction mayoccur in a variety of circumstances in patients with coronary artery disease. Barring an intraventricular conduction disorder, transient Q waves usually reflect intense but reversible myocardial ischemia, requiring aggressive therapy to salvage myocardium in jeopardy. Q waves may also disappear months or years after a Q-wave myocardial infarction but rarely in the acute or subacute phase. Transient Q waves have assumed greater importance because of the current therapy of myocardial infarction and ischemia with thrombolytic agents, angioplasty, and coronary bypass surgery.

We studied the occurrence and characteristics of crosstalk related to the atrial sense marker function of the Intermedics Cosmos DDD pulse generator in 29 patients. Upon activation of the atrial sense markers, the pulse generator delivers a series of markers in the form of triggered atrial stimuli at 0.025 ms in duration at the programmed voltage output of the atrial channel. Under certain circumstances, these atrial sense marker stimuli may cause crosstalk when they are sensed by the ventricular sensing amplifier. This form of crosstalk may be eliminated in most cases by decreasing ventricular sensitivity and/or atrial output voltage.

Normally functioning DVI pulse generators with different electronic characteristics may cause complex cardiac arrhythmias that must not be interpreted as pacemaker malfunction. When there is no refractory period after the atrial output, a DVI pulse generator may deliver atrial pacemaker impulses at irregularly shortened intervals and produce an increase in the atrial pacemaker rate compared with the programmed free-running AV sequential rate. Theoretically this variation of the atrial cycle length can occur only within a well-defined range that represents the difference between the ventricular and atrial output escape intervals. In reality, the interplay of the spontaneous sinus rate, duration of AV conduction, time of sensing the ventricular electrogram in relation to the surface QRS complex, and the programmed AV sequential time all influence the atrial pacemaker rate. DVI pulse generators may also create interesting arrhythmias such as pseudopseudofusion beats (delivery of an atrial spike within the QRS complex), double pseudofusion beats, and double pacemaker impulses within the QRS complex according to the electrophysiologic circumstances and specifications of the pulse generator.

This report describes the use of chest wall stimulation (CWS) for the termination of ventricular tachycardia in two patients with dual chamber pulse generators functioning in the DDD mode. Rapid CWS induced burst ventricular pacing when CWS was selectively sensed by the atrial channel, whereupon the pulse generator triggered its ventricular output. In this way, by programming the pulse generators to the maximum upper rate, this CWS technique produced burst ventricular pacing at a rate of 175 to 180/minute that successfully terminated ventricular tachycardia in both patients. The same CWS technique also initiated ventricular tachycardia by burst ventricular pacing. This CWS technique may be useful for the termination of relatively slow ventricular tachycardia in patients with DDD pulse generators when the maximum rate of ventricular pacing cannot be otherwise increased.

Purpose: Pacemaker endless loop (or reentrant) tachycardia (ELT) is often terminated by conversion to the asynchronous mode of pacing by simply placing a magnet over the implanted atrial tracking (DDD or VDD) pacemaker. We investigated three other simple methods of ELT termination—chest wall stimulation (CWS), provocation of myopotential oversensing, and chest thumping—that may be useful when the arrhythmia is unresponsive to magnet application or a magnet is unavailable. Patients and methods: A modified CWS technique using an external pulse generator (pulse width=40 msec) ordinarily used for transcutaneous cardiac pacing was tested in 74 patients (40 with unipolar and 34 with bipolar DDD devices). CWS inhibited the ventricular channel of all DDD pacemakers easily and reliably. CWS was then applied during ELT in 20 patients (10 with unipolar and 10 with bipolar DDD devices). Provocation of myopotential oversensing by the ventricular channel was attempted during ELT in 10 patients with unipolar DDD pacemakers. Chest thumping was tried during ELT in six patients. Results: CWS by the modified technique terminated ELT in all patients in whom the arrhythmia was induced. Myopotential oversensing resulted in successful ELT termination in six of the 10 patients. ELT was successfully terminated by chest thumping in four of six patients. Conclusion: These simple techniques provide effective ways of ELT termination other than magnet application, and may be easily applied by physicians unfamiliar with the complexities of contemporary DDD pacemakers and their programmers.

The diagnosis of myocardial infarction during ventricular pacing can be made in a substantial number of patients, mostly by applying the diagnostic criteria that are useful in the presence of complete left bundle branch block. There are, however, important exceptions to this general rule during ventricular pacing, and normal depolarization patterns must be recognized to avoid the erroneous diagnosis of myocardial infarction.

A low pressure gradient across the residual lesion and a minimal percent residual stenosis are markers of a successful coronary angioplasty. A more physiologic method of assessing the results of coronary angioplasty would involve assessment of myocardial perfusion in the affected coronary bed. Contrast two-dimensional echocardiography provides information about regional myocardial perfusion. To assess the correlation between pre- to postcoronary angioplasty changes in gradient or percent stenosis and the increase in peak contrast intensity, 23 consecutive patients were studied during coronary angioplasty. In 19 of the 23 patients, the coronary angioplasty was successful and in 15 (79%) of the 19, an adequate echocardiographic study was obtained. Mild and transient side effects of echo contrast were observed in 3 of the 15 patients. The gradient across the residual lesions decreased from 52 +/- 12 to 11 +/- 4 mm Hg (mean +/- SD), the diameter of the stenotic lesion decreased from 89 +/- 10 to 25 +/- 16% and corrected peak contrast intensity (peak contrast - baseline contrast in gray level U/pixel) increased from 15 +/- 16 to 50 +/- 26. All these differences were significant at the p less than 0.001 level. Corrected peak contrast intensity correlated exponentially with the decrease in pressure gradient (r = 0.82, p less than 0.001). The correlation curve had a greater increase in peak contrast intensity at gradient decreases greater than 45 mm Hg. Corrected peak contrast intensity did not correlate with decrease in diameter of the stenotic lesion (r = 0.19).

Sonicated albumin has been proposed as a near ideal echocardiographic contrast agent with little myocardial toxicity or hemodynamic effect. Its use has not yet been reported in humans, partly because of difficulties in preparation. With use of the newly modified sonication method, 10 ml of 5% albumin was sonicated for 75 s with a 5.0 ml slow infusion of air. This resulted in microbubbles with a mean diameter (+/- SD) of 5 +/- microns). Fourteen patients undergoing routine coronary angiography were studied. One patient had normal coronary arteries; the other 13 had significant coronary artery disease. In a subgroup of nine patients, sonicated albumin and sonicated diatrizoate meglumine sodium (microbubble diameter 9 +/- 3 microns) were injected several minutes apart, using the same technique. Videodensity-time curves were obtained from a region of interest in the myocardium. Corrected peak contrast intensity (baseline contrast intensity subtracted from peak contrast intensity, gray scale U/pixel) for sonicated albumin and for sonicated diatrizoate meglumine sodium was 51 +/- 26 and 52 +/- 19, respectively (p = 0.89). Washout half-time (T1/2) for the two agents was 5.5 +/- 4.5 and 16.0 +/- 12.2 s, respectively (p = 0.01). One patient with unstable angina experienced transient chest pain after repeated albumin injections. No electrocardiographic changes, blood pressure changes or wall motion abnormalities were observed. Administered by intracoronary injection, sonicated 5% albumin is a safe and effective echocardiographic contrast agent for myocardial perfusion imaging, yielding excellent myocardial contrast with physiologic washout time.

We are describing a case of atrial septal aneurysm (diagnosed by echocardiography), systolic click and atrial tachyarrhythmia. The implications of these findings are discussed.

This report describes hyperkalemia-induced failure of atrial capture associated with preservation of ventricular pacing in a patient with a dual-chamber (DDD) pacemaker. This differential effect on atrial and ventricular excitability during cardiac pacing correlates with the well known clinical and experimental observation that the atrial myocardium is more sensitive to hyperkalemia than is the ventricular myocardium.

This report describes two cases of double sensing of the P and QRS signals by an implanted atrial bipolar automatic burst tachycardia-terminating puise generator (Inlermedics CyherTach 60) used for the treatment of supraventricular tachycardia. Double sensing occurred during normai sinus rhythm at a rate slower than the tachycardia detection criterion and caused inappropriate delivery of burst stimulation. These observations underscore the importance of the far-field QRS signal in the detection of supraventricular tachycardia by automatic puise generators sensing the atrial eiectrogram.

An important complication of temporary cardiac pacing by the transfemoral approach. This report describes three cases of inapparent double puncture of the femoral artery and vein as a complication of the transfemoral approach for temporary cardiac pacing. This complication may lead to the passage of a pacing catheter to the right ventricle by way of the femoral artery and vein and may remain undiagnosed until the rigid outer sheath of the introducer set is withdrawn over the pacing catheter. Therefore, we recommend immediate withdrawal of the rigid outer sheath as soon as the catheter lies freely in the iliac vein or the inferior vena cava. If double puncture has occurred, arterial blood will leak around the pacing catheter. Control of arterial bleeding by local compression should not be attempted without removal of the pacing catheter.

Diaphragmatic myopotential inhibition in multiprogrammable pacemakers was tested in 119 patients with implanted devices from six different manufacturers. There were 105 VVI pulse generators (46 bipolar and 59 unipolar) and 14 unipolar DVI pulse generators. Diaphragmatic myopotential inhibition was tested by observing the effect of a maximal deep inspiration in the supine position with the pulse generator programmed at various sensitivities. Inhibition was demonstrated in four of 46 bipolar VVI units (8.7%) and twelve of 59 unipolar VVI units (20.3%). Inhibition was also demonstrated in four of 14 unipolar DVI systems from the one manufacturer (28.6%). This form of interference appears to be a benign clinical problem and rarely if ever leads to prolonged asystole. It should be considered in the differential diagnosis of pacemaker pauses, particularly in patients with multi programmable pulse generators programmed at higher sensitivities.

This paper describes our approach to the interpretation of electrocardiograms produced by a new unipolar multiprogrammable “committed” DVI pulse generator (Intermedics) during normal function. The arrhythmias engendered by this new DVI pacemaker may be better understood by conceptualizing the recycling mechanism in terms of a simple atrial pulse generator with two important qualifica-tions: (1) the ventricular stimulus obligatorily follows the atrial stimulus after 155 ms (AV sequential interval); (2) the pulse generator senses ventricular events (via the ventricular electrode) but recycles according to its atrial timing cycle (AA interval). These characteristics lead in turn to two important consequences: at the QA interval (from the onset of a sensed QRS complex to the succeeding atrial stimulus) must be longer than the VA interval (from a ventricular stimulus to the succeeding atrial stimulus) by a period equal to or slightly greater than the AV sequential time. This may be considered to represent a form of bysteresis, by the pacemaker refractory period always starts at the onset of an atrial cycle (AA interval) and therefore occurs after the delivery of an atrial stimulus or after a sensed ventricular event. The above characteristics may cause pacemaker stimuli to fall within the P wave, PR interval, QRS, ST segment and the ascending limb of the T wave during normal function of the pulse generator. Superficially, these peculiarities resemble malfunction and may be quite befuddling but they all occur predictably according to the electronic design of the pulse generator. (PACE, Vol. 4, November-December, 1981)

The evaluation of pacemaker function may be quite perplexing when a demand (ventricular-inhibited) pulse generator senses intracorporeal voltages invisible on the standard 12-lead electrocardiogram (ECG). These signals may originate from the T-wave, the pacemaker system itself, skeletal muscle potential, and according to some workers from concealed ventricular extrasytoles.

Chest wall stimulation may be used diagnoslically and therapeutically in the follow-up of patients with automatic tachycardia-terminating pulse generators. In this report, we present our experience with chest wall stimulation in the follow-up of five patients with implanted Intermedics CyberTach 60 automatic tachycardia-terminating pacemakers (three for supraventricular tachycardia and two for ventricular tachycardia). Chest wall stimulation delivered at a rate faster than the rate detection criterion of the pulse generator often precipitates reentry tachycardia, making it possible to perform a noninvasive electrophysiologic study. In addition, chest wall stimulation may be invaluable in the termination of reentry tachycardia which is unsensed by an implanted pulse generator either because the rate is too slow, or below the rate detection criterion, or because the intracardiac signal does not attain the sensitivity of the pulse generator.

The echocardiographic features of a tumor in the right ventricular outflow tract that prolapsed into the pulmonary artery during systole are described. The patient was a 19 year old woman who presented clinically with bacterial endocarditis involving a mildly stenotic pulmonary valve. An echocardiogram, obtained to evaluate the pulmonary valve for bacterial vegetations, showed abnormal echoes throughout the cardiac cycle; they suggested a tumor mass in the right ventricular outflow tract in front of the pulmonary valve with possible extension into the pulmonary artery during systole. Additional tumor echoes confined to diastole were recorded in front of the aortic root and the tricuspid valve. These features were further elucidated with a computer-generated two dimensional cineechocardiogram that clearly showed a portion of the tumor mass passing beyond the position of the pulmonary valve into the main pulmonary artery in systole and returning into the right ventricular outflow in diastole. At surgery, a large myxoma was found in the right ventricular outflow tract with a polypoid extension that projected into the pulmonary artery in systole and contained a fibrinous vegetation at its tip. The left cusp of the pulmonary valve was normal, but the other two leaflets showed evidence of endocarditis.

The recent release ofDDD (and VDD) pulse generators with relatively short atrial refractory periods has set the stage for the development of endless loop or electronic reentry tachycardias because of the frequent occurrence of retrograde V A conduction in patients requiring permanent pacing. The absence of VA conduction during electrophysiologic testing at the time of implantation does not necessarily predict protection against endless loop tachycardia because VA conduction may occasionally become manifest only after implantation. Programmability of the atrial refractory period constitutes the most important pacemaker characteristic for the prevention of endless loop tachycardia. We have found chest wall stimulation a useful technique for the verification of the programmed upper atrial tracking rate, duration of the pacemaker atrial refractory period, and characterization of the predicted response to the upper programmed rate. Chest wall stimulation can initiate and terminate endless loop tachycardia in patients predisposed to this arrhythmia.

Summary The electrocardiographic diagnosis of myocardial infarction in patients with ventricular pacemakers is often difficult. This report describes the electrocardiograms of two patients with permanent ventricular pacemakers in whom the diagnosis of acute anterior myocardial infarction could be made with confidence by observing the evolution of primary ST and T wave abnormalities in the absence of specific QRS changes.

Excerpt Several studies have proved the usefulness of echocardiography in the diagnosis of dissecting aneurysms involving the aortic root (1-5). The main findings include increased width of the aor...

Two patients with Omni-Stanicor pulse generators presented an apparent sensing problem characterized by intermittent reversion to fixed-rate pacing only during atrial fibrillation with a very rapid ventricular rate. Every fixed-rate cycle contained two unsensed beats. The first unsensed beat fell in the noise sampling period (the last 1/6 of the pacemaker refractory period) and, therefore, disabled the demand function of the pulse generator for a single timing cycle. The presence of two consecutively unsensed beats within one timing cycle (automatic or escape interval) during tachycardia suggests normal function of the noise sampling period of this particular pulse generator, rather than a true sensing problem. The diagnosis becomes evident if the sensing problem disappears when abbreviation of the refractory period occurs by reprogramming the pulse generator at a higher rate.

The diagnosis of inferior wall myocardial infarction is often masked during ventricular pacing. We observed paced ventricular beats with a qR pattern in leads 2, 3, and aVF in a patient with acute inferior wall myocardial infarction and a temporary pacemaker at the apex of the right ventricle. Such a pattern might be specific for the diagnosis of inferior wall myocardial infarction, because it is never seen during uncomplicated pacing from anywhere within the right ventricular cavity.

Endless loop tachycardia is a well-known complication of DDD pacing and is almost invariably terminated by conversion to the asynchronous DOO mode upon application of a magnet over the pulse generator. Occasionally magnet application is ineffectual because the ventriculoatrial (VA) synchrony of endless loop tachycardia is converted directly or indirectly to an atrioventricular (AV) desynchronization arrhythmia, another form of VA synchrony. This occurs when a paced ventricular beat engenders an unsensed retrograde P wave and the continual delivery of an ineffectual atrial stimulus during the atrial myocardial refractory period creates self-perpetuating VA synchrony. Upon magnet removal, AV desynchronization arrhythmia reverts immediately to endless loop tachycardia. In the absence of access to programmers, magnet unresponsive endless loop tachycardia can be easily and reliably terminated by chest wall stimulation through inhibition of the ventricular channel of the DDD pulse generator.

This report describes the electrocardiograms of a patient with an intermittent electrode fracture presenting with periodic attenuation of the pacemaker spike without loss of ventricular capture. There was infrequent prolongation of the spike-to-spike interval probably because the pulse generator interpreted random false signals as interference and reverted to its fixed-rate mode. These observations add to the spectrum of electrocardiographic abnormalities of electrode malfunction.

This report describes the Jong-term follow-up of two patients who received implantable automatic burst tachycardia-terminating ventricular pacemakers for the treatment of drug-refractory sustained ventricular tachycardia. After implantation, both pulse generators continued to terminate ventricular tachycardia without any major complications. In one patient, after three years, many episodes of ventricular tachycardia were slower than the tachycardia-detection criterion rate of 137 per minute; ventricular tachycardia was then terminated by chest wall stimulation that activated the burst function of the pacemaker. In this particular patient, the pulse generator was removed after four and one-half years and replaced with a DDD system because of the pacemaker syndrome and attacks of ventricular tachycardia, often at a rate of about 100/minute. In the second patient, the pacemaker continued to terminate ventricular tachycardia for over five and one-half years as determined by the repeated activation of the flag (memory) function of the pacemaker indicating detection of tachycardia by the pulse generator and resultant delivery of burst pacing.

The widespread use of cardiac pacemakers [1] has added a new dimension to clinical electrocardiography because about 99% of all cases of pacemaker malfunction can be detected with the conventional electrocardiogram (ECG). This chapter outlines our approach to the problem of pacemaker malfunction (Table 1) with emphasis on some of the newer concepts. The large variety of pacemaker models from a proliferating number of manufacturers has rendered the subject increasingly complex.

Identifying molecular cancer drivers is critical for precision oncology. Multiple advanced algorithms to identify drivers now exist, but systematic attempts to combine and optimize them on large datasets are few. We report a PanCancer and PanSoftware analysis spanning 9,423 tumor exomes (comprising all 33 of The Cancer Genome Atlas projects) and using 26 computational tools to catalog driver genes and mutations. We identify 299 driver genes with implications regarding their anatomical sites and cancer/cell types. Sequence- and structure-based analyses identified >3,400 putative missense driver mutations supported by multiple lines of evidence. Experimental validation confirmed 60%–85% of predicted mutations as likely drivers. We found that >300 MSI tumors are associated with high PD-1/PD-L1, and 57% of tumors analyzed harbor putative clinically actionable events. Our study represents the most comprehensive discovery of cancer genes and mutations to date and will serve as a blueprint for future biological and clinical endeavors. A comprehensive analysis of oncogenic driver genes and mutations in >9,000 tumors across 33 cancer types highlights the prevalence of clinically actionable cancer driver events in TCGA tumor samples., 0, info:eu-repo/semantics/published