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Dear Sir, We thank Drs Muller-Nordhorn and Willich for their interest in our paper. They critically question the validity of our conclusion that the Framingham risk function overestimates risk of coronary heart disease in men and women from Germany. Firstly, they assume a potentially strong healthy worker effect among the participants of the PROCAM study. It is worth noting that the estimate they present for this effect—25% lower cardiovascular risk-was derived in a group of industrial workers where selective forces in favour of the physically healthy, at hire and by time on employment, is known to be particularly pronounced. However, …

I read with interest the paper by Ronner et al. and the editorial by Mahadevan et al.1,2 In their article the authors have presented a single-centre retrospective study of patients who were admitted or transferred with myocardial infarction and underwent rescue therapy within 24 h for failed thrombolysis. In this study three rescue therapies were used after failed thrombolysis (PCI 74%, re-thrombolysis 39%, and GP IIb/IIIa receptor blockers 53%). The incidence of bleedings was increased in all combination rescue groups. …

We read with interest the recent paper by Colivicchi et al., whichreported on the clinical presentation, diagnostic work-up and long-term outcome of a consecutive series of elite athletes (n=33) with recurrent exercise-related syncope (ERS).1 The athletes were referred to the authors' syncope clinic after 12-lead ECG and transthoracic echocardiography. The only structural heart disease detected was mitral valve prolapse with mild mitralregurgitation in two individuals. Subsequently, Holter monitoring, exercise testing, electro-encephalography, electrophysiological testing and head-up tilt testing were performed, although the numbers of each investigation performed was not stated. Most of the athletes (66%) had a positive …

The purpose of this paper is to investigate whether the inhibitory action of purinic compounds (striadyne: STR) on the sinus node is quantitatively different on a pathological sinus node in comparison to a normal one and thus whether it is possible, as suggested by other authors, to use STR as a pharmacological test in the diagnosis of sick sinus syndrome (SSS). With this aim we investigated 55 patients, divided into 3 groups according to ECG and sinus function evaluation tests: 1--normal; 2--SSS (2a: flagrant SSS; 2b: latent SSS); 3--excess vagotonia and/or abnormal response to vagal stimulation. In all patients after a prophylactic insertion of a temporary pacemaker, 30 mg of STR were rapidly injected i.v. and the surface and intracavitary ECG continuously recorded until the basal state was regained; the following parameters were evaluated: average baseline sinus cycle (SC), minimum and maximum SC after the drug. In all patients STR caused first a slowing, then an acceleration of the sinus rate. SC lengthening was moderate in groups 1 and 3 [max SC was respectively 740-1820 ms (1198 +/- 290.9 ms) and 720-1440 ms (1157.5 +/- 223.3 ms)], but it was severe in patients with SSS [max SC in group 2a 2500-11880 ms (5398.3 +/- 2687.4 ms) in group 2b 1620-11140 ms. (4470.7 +/- 3660.6 ms)]. The difference between the max post STR SC of SSS patients, and the control group was highly significant P less than 0.001). Assuming as upper limit of the normal a value of 2071 ms. (corresponding to the mean + 3 standard deviations of the response of the control group) we recorded abnormal responses in 100% in group 2a and in 85.7% in group 2b, whereas there were no abnormal responses in group 3. In addition, nodal atrioventricular block occurred frequently. The authors believe this test could be useful in the diagnosis of SSS, but it is essential to insert a ventricular pacing catheter prophylactically if this test is used.

Treatment of a patient with myocardial infarction might include opiates and sedatives to reduce pain and anxiety, heparin, antiarrhythmic drugs, diuretics which aim at improvement of myocardial function and drugs which might reduce the ischemic area at risk and thus mortality such as beta-blockers, vasodilators and possibly calcium antagonists. Obviously a selection of these and other therapeutic agents should be made for each individual patient. Guidelines for such a selection are presented in this paper. These are based on assessment of the hemodynamic state in a given patient: heart rate, blood pressure and presence or absence of heart failure as determined by non-invasive examination or by hemodynamic monitoring with a pulmonary artery catheter. An attempt should be made to reach an optimal hemodynamic state quickly, preferably within one hour of admission to the coronary care unit: a heart rate between 60 and 80 b.p.m., a systolic blood pressure between 100 and 140 mmHg and absence of signs of heart failure. For this purpose fast-acting intravenous drugs should be employed. Possibly myocardial preservation could also be achieved by prompt recanalization of an occluded coronary artery. At present, however, this is still an experimental procedure which should be further investigated.

Echocardiography is a very useful non-invasive method of cardiac diagnosis. It has been widely used in evaluating the effects of some drugs, such as nitrates[1–7], prazosin[8,9], and propranolol[10], on heart and seems very successful. In this paper, the echocardiographic studies of the effects of nitrates on left ventricular dimension and volume have been reviewed and an attempt has been made to answer whether or not echocardiography can allow to monitor the effects of nitrates in patient groups and further in individual patients.

Right ventricular dysplasia (RVD) is a cardiac anomaly characterized by replacement of right ventricular myocardium by adipose and fibrous tissue that was first described at autopsy, and is now being recognized pre-mortem. Sudden death and ventricular arrhythmias are the most common clinical manifestation of the condition. This paper reviews the literature on myocardial biopsies performed in patients with idiopathic arrhythmias who had pathologic findings consistent with RVD, and the results of biopsies from patients suspected of having RVD. The significance of sampling error in myocardial biopsies, possible familial associations, and other conditions associated with myocardial adipose infiltration are also discussed. Based on the review, the possibility is raised that RVD may represent the end result of an unusual healing process, whereby genetically susceptible individuals recover from a variety of RV insults by deposition of adipose tissue. These fatty scars may then be the focus for arrhythmias which remain the major clinical manifestation of the syndrome.

Irrespective of age or species, injured cardiac myocytes accumulate Ca2+. In this paper four different aspects of the Ca2+-overloading phenomenon are discussed. These aspects include the conditions under which it occurs, the possible routes of Ca2+ entry, the metabolic consequences of the raised tissue Ca2+ and possible protective procedures. The particular protective procedures that will be described involve the combined use of hypothermia and nifedipine (50 micrograms/l), with and without K+-induced chemical cardioplegia. Isolated, electrically paced rabbit hearts were made ischaemic for 60 to 180 min at 37, 28, 25, 15, 12 and 5 degrees C and then reperfused at 37 degrees C. In some experiments nifedipine was added to the perfusion buffer, with and without K+-induced cardioplegia. Recovery was assessed in terms of recovery of mechanical function, maintenance of the tissue stores of adenosine 5'-triphosphate (ATP) and creatine phosphate, and maintenance of the ATP-generating activity of the mitochondria. These results show that the cardioprotective effects of nifedipine and hypothermia are additive.

Reperfusion of an ischaemic region in the dog heart has several possible consequences for the affected myocardium. The relative importance of each of these consequences depends on the severity and duration of blood flow deprivation, on whether the myocytes have been reversibly or irreversibly injured and on whether injury to the microvasculature has occurred. In this paper, the following important effects of reperfusion in ischemic myocardium are reviewed: (1) The acceleration of the disintegration of irreversibly injured myocytes by reperfusion results in contraction band necrosis. The sarcolemmal damage associated with this phenomenon permits accelerated washout of creatine kinase and other intracellular constituents. (2) Haemorrhage into the area of ischaemic injury results from reperfusion of tissue exhibiting severe ischaemic vascular injury. (3) Potentially fatal arrhythmias may be initiated by reperfusion. (4) Myocardial salvage occurs and infarct size is limited if reperfusion is instituted at a time when reversibly injured ischaemic myocytes at risk of necrosis are still present. In dogs there is a transmural ‘wavefront’ progression of irreversible ischaemic injury which occurs as a function of increasing duration of ischaemia; thus, the logical goal of very early reperfusion is complete prevention of celldeath and that of later reperfusion is the conversion of what might have been a transmural infarct to a nontransmural or subendocardial infarct. The time within which reperfusion can limit infarct size in experimental models of infarction is about 3 h. In some animals, small amounts of salvageable myocardium may persist beyond 3 h, but limitation of infarct size has not been demonstrated experimentally beyond 5–6 h. (5) Metabolic and functional recovery of surviving myocytes may require several days. Thus, the functional benefits of reperfusion may be underestimated if evaluated immediately after reperfusion.

Understanding of the factors affecting regurgitant flow through a heart valve and of the inherent limitations of the Doppler technique is needed to interpret correctly the information obtained during an ultrasound Doppler examination. This paper describes the flow conditions at the leaking valve and limitations of the Doppler technique which become important in the case of valve regurgitation. The flow conditions can be described in the following terms: contraction of the flow, core flow dimensions, friction, and intrusion and width of the jet flow. Contraction occurs at the entrance to the orifice and causes the width of the jet at the orifice to be smaller than the orifice itself. This contraction should be taken into account when calculating volume flow. The jet reaches a minimal area at the vena contracta where the flow velocity is close to that expected from the Bernoulli equation. The area of the vena contracta relative to the area of the hole can vary between 0.6 and 1.0; the lowest value is seen at a sharp-edged orifice and the highest value, at a hole with an ideally rounded inlet. Friction has a marginal role on flow velocity at the vena contracta. The velocity at the vena contracta persists in a region called the core flow region. This region has a length of 4-8 hole diameters. The total jet intrusion and the width of the jet are related to both the flow velocity at the hole and the diameter of the hole.(ABSTRACT TRUNCATED AT 250 WORDS)

In the following paper different aspects of left ventricular hypertrophy (LVH) will be reported, which demonstrate two aspects of LVH in cardiomyopathies: firstly, the role of LVH in cardiomyopathies differs from that of LVH in other myocardial diseases {see classification and etiology, appearances of LVH, functional course), and secondly, LVH implies a great variety of features, which seem to be of clinical and theoretical importance (see morphology, hypertension, therapy).

In this paper we have extrapolated from data on the general population of middle-aged men and made suggestions for risk prediction and prevention policy in aircrew. As suggested previously, it would be helpful in future if data on the risk of heart attack in pilots could be generated from a central recording system covering both current pilots and those who retire for whatever reason. Indefinite follow-up information on ischaemic events would also be particularly helpful.

This paper describes a protocol of assessing specific working fitness of post-myocardial infarction patients proposed by the Italian Committee on Occupational Cardiology. After cardiovascular (cross-sectional echocardiography, Holter monitoring and maximal symptom-limited ergometric test) and psychological evaluation (CBA-2.0), two ambulatory ECGs were used during work to confirm the first judgement of specific work fitness expressed by occupational specialists. The preliminary results obtained in 106 uncomplicated male patients (mean age 49 +/- 8 years) show that: (i) return to work (89.6%) at 117 +/- 51 days after the acute event is mainly related to socio-occupational variables rather than to cardiovascular status; (ii) the results of the ambulatory monitoring usually confirm the first judgment of specific work fitness; (iii) heart rate responses recorded during work are unrelated to the judgment of fitness; and (iv) the repeatability of the results observed during the two ambulatory ECGs at work is good.

In patients with unstable angina pectoris, transient episodes of ischaemia occur frequently and the prognostic implications of those predominantly silent episodes have been shown. The method of Holter tape recording is, however, not ideal for the care, of unstable patients: (a) the results of a recording period are only available after this period is finished and subsequent evaluation has taken place; and (b) the sensitivity of monitoring may be increased by recording more than two leads. We have used a portable ECG computer, which monitors the 12-lead ECG every 20 s and records ECGs either when there is consistent ST deviation or at preset intervals (1,3,5 min). It stores the information on solid-state memory and displays a summarized ST-level trend on a monitoring screen. The stored information can be reviewed at any time at the bed-side and selected ECGs can be printed out on paper. We have evaluated this device in 23 patients on our CCU, with unstable angina (10), evolving myocardial infarction (4) and post PTC A (9). Forty-two consecutive trend recordings were controlled with independent visual interpretation of 2920 complete 12-lead ECGs. Deviations of the ST-level trend of less than 0.1 mV were due to artefact in over 95%. However, when the ST-level trend showed deviations of above 0.1 mV, 93% of the 12-lead ECGs showed true pathologic changes. Eighty-two per cent of the recorded episodes of transient ischaemia were silent; angina was in every case preceded by ECG changes. In four patients the on-line recorded ECG was instrumental for the decision towards acute angiography, PTCA or bypass-operation. We conclude that: (1) programmed 12-lead ECG recording allows early on-line detection of myocardial ischaemia; (2) the sensitivity of the ST-level trend to detect pathologic ECG changes at 0.1 mV is 93%; (3) the specificity is above 95% for changes exceeding 0.1 mV.

In this paper we report the sequelae of a patient with an anomalous right coronary artery (RCA) originating from the pulmonary artery (PA) in association with a normal heart, operated upon at the age of 13 years. Three years after the end-to-side reimplantation of the RCA, with a rim of the PA, into the aorta, the surgical result has been evaluated by cineangiography. Before operation both coronary arteries were tortuous and increased in size. Afterwards the left coronary artery showed a normalized calibre, although the RCA remained tortuous with no decrease of the internal diameter. The notable postoperative changes in shape and size of the LCA may be due to the disappearance of the steal phenomenon. The lack of involutive changes in the RCA could be explained by its thinner wall. Left ventricular wall motion, evaluated under resting conditions and during an atrial pacing stress test, was found to be normal.

In the Rotterdam system of prehospital care for patients with circulatory failure, the cardiopulmonary resuscitation (CPR) training programme for lay persons contributes to the first link in the chain of care, i.e. the period of time spent awaiting the arrival of professional staff. In this paper we describe some of the medical aspects of this programme. The material used was obtained in a study of 5312 trainees who had followed a CPR course. Case histories were reconstructed of 91 victims who had been resuscitated by 109 respondents. At least 20% of resuscitated persons had collapsed as a result of non-cardiac causes. In this category the longer term survival rates were relatively the most favourable. In several instances the indication for resuscitation had been incorrect, while the technical proficiency in the delivery of CPR was often inadequate. We conclude that one course is insufficient for the development of the required 'skill'. We also conclude that the courses should dwell more elaborately on the non-cardiac causes of collapse, particularly in training programmes addressing the public at large. Attention is drawn to the need of designing and implementing special courses for family members and relatives of persons known to be cardiac patients. The need for continuing evaluation, involving active contributions from lay resuscitators, is underlined.

The accepted rationale for the use of beta-adrenoceptor antagonists in the therapy of angina pectoris is that these drugs, by inhibiting the positive chronotropic and inotropic effects of sympathetic stimulation, reduce the myocardial oxygen consumption. In the present paper, another aspect of these agents, namely the effect on blood supply to the jeopardized myocardium, is discussed. In the presence of coronary artery stenosis, transmural blood flow to the ischaemic zone may be reduced and the endocardial perfusion, reactive hyperaemia and the contractile function of the myocardium are significantly affected. The administration of beta-adrenoceptor antagonists reduces the heart rate, myocardial contractility and myocardial oxygen demand, and improves the biochemical, electrical and mechanical function of the jeopardized myocardium, particularly during exercise or stress. The transmural blood flow may or may not increase but there is usually a redistribution of blood flow in favour of the endocardium where the imbalance between oxygen demand and supply is most marked. The main mechanisms responsible for this favourable redistribution appear to be: (i) an increase in the diastolic period, particularly in relation to the cardiac cycle, (ii) a restoration of autoregulation in the epicardium, and (iii) a vasoconstriction mediated by beta-adrenoceptors. The improvement of endocardial perfusion may play an additional role in the salvage of jeopardized myocardium.

The quality of 269 research ambulatory ECG recordings was evaluated. Nine recordings failed for technical reasons, and 20 others had a high noise level making them unsuitable for research purposes. The remaining 240 or 89% of the recordings were considered satisfactory. Evaluation of a semi-automatic ECG analyser (Reynolds Pathfinder) revealed an overall accuracy of QRS complex detection of 98.9% (range 84.3–100%). Except for six recordings with great variability in QRS morphology more than 95% of detected QRS events were classified as normal or aberrant. Artifacts gave rise to ≥1 false positive pause per 1000 QRS events in 23% of the recordings. Ventricular premature beats (VPBs) detected solely by their aberrancy gave rise to a high number of false positive VPBs per recording (mean: 333, range: 4–2613). When VPBs were detected by their prematurity as well, these figures were reduced (mean: 94, range: 0–572). The number of false negative VPBs (‘missed VPBs’) was evaluated in 18 recordings with a mean of 1639 (range: 172–6660) VPBs per 24 h documented on paper. The number of VPBs missed by the computer was on average 5% (0–40%) when VPBs were detected as premature aberrant events. Only in four of these cases was this percentage significantly reduced, when VPBs were detected solely as aberrant events. This variability in quality of ambulatory ECG recordings and performance of arrhythmia computers underscores the need for a quality control procedure, when semi-automatic analysis of ambulatory ECG recordings are used for research purposes.

The aim of this paper is to describe various positive inotropic drugs (except the cardiac glycosides) and to attempt a classification according to their mechanism of action. The most important drugs with established positive inotropic effect are summarized first. Present interest focuses on the development of new agents with sufficiently high oral bioavailability and long duration of action. Prenalterol is a beta 1-adrenergic drug which appears to fulfil these criteria. Of increasing importance are drugs which combine a positive inotropic and a vasodilator effect. These include mainly the methylxanthines and possibly also the beta 2-adrenoceptor stimulating agents salbutamol, terbutaline, fenoterol and pirbuterol. A positive inotropic and vasodilator effect is also produced by the new compounds amrinone and AR-L 115 BS. These drugs appear to resemble theophylline and other methylxanthines in that they also act mainly as phosphodiesterase inhibitors with a subsequent increase in cAMP without interference with alpha- or beta-adrenoceptors. The mechanism of the as yet only experimentally established positive inotropic effect of alpha-adrenoceptor stimulating agents, e.g. phenylephrine, is unknown. However, it is independent of the cAMP system and is not accompanied by changes in frequency.

This paper summarizes the effects of various drugs (sodium channel inhibitors, alpha and beta-adrenoceptor blocking agents, calcium antagonists and substances that interfere in various ways with the metabolism of arachidonic acid (e.g. aspirin, dazoxiben, nafazatrom) on the early consequences of experimental acute myocardial ischaemia. Particular attention is paid to effects on the serious early arrhythmias that arise within a few minutes of the onset of ischaemia, on those ventricular arrhythmias that result from the subsequent reperfusion of the ischaemic myocardium and on the severity and extent of myocardial ischaemic damage. From these experimental studies conclusions are drawn regarding possible approaches to early intervention with drugs in clinical myocardial infarction. Among those agents where, based on results from studies in animals, early administration should prove beneficial are beta-adrenoceptor blocking drugs, calcium antagonists, drugs that inhibit thromboxane synthesis or its effects at receptor level, agents that 'promote' prostacyclin, nitroglycerin and analgesics with marked antiarrhythmic properties (e.g. meptazinol). However, the answer to the question as to which (if any) of these drugs should be given early in clinical infarction is still dependent upon the results of considerably more experimental and clinical studies.

Bacterial endocarditis still remains a serious disease with significant morbidity and mortality. In patients with known valve disease, most cases are caused by oral viridans streptococci. These organisms are present in vast numbers on the gum margins and in gum pockets. They cause transient bacteraemia during eating and tooth brushing. More substantial, but short-lived bacteraemia can occur during dental treatment such as extraction and scaling. Bacteria may then become attached to abnormal endocardium leading to the development of infective endocarditis. Prophylaxis of endocarditis during dental procedures in patients with known valve disease should thus be aimed at reducing the number of bacteria entering the blood stream and eliminating those that get there. This can be sought first by good oro-dental hygiene and secondly by the use of prophylactic antibiotics. In this paper, we set out simple guidelines for practitioners in those countries that do not already have recommendations of their own. They are based on guidelines already in use in the United Kingdom, France, Switzerland and the United Stated(1–4)

This paper describes the two-dimensional echocardiographic and pulsed Doppler findings in a 25-year-old man with tricuspid insufficiency due to carcinoid heart involvement. A hypothesis explaining the time sequence of the carcinoid valve involvement is suggested.

This paper discusses the relevance of certain animal models for the production of ischaemia and reperfusion-induced ventricular arrhythmias to clinical problems of ischaemia, for example, sudden cardiac death. It then describes experiments in anaesthetised rats subjected to acute coronary artery occlusion in which nifedipine (administered both intravenously and orally) prevented the occurrence of ventricular fibrillation and markedly increased survival. In anaesthetised dogs, a continuous intravenous infusion of nifedipine reduced the severity and incidence of ventricular ectopic activity and also dramatically improved survival on reperfusion from 12·5% (in the controls) to 88%. The mechanisms of this protection are discussed.

In this paper the effects of beta blockade on renal haemodynamics are reviewed. Although renal blood flow often declines during treatment with beta-blocking drugs, in many cases it is possible to demonstrate relative or absolute vasodilation in the kidney. Renal vasoconstriction seems to be a predominant pattern in patients who do not exhibit a hypotensive response. The mechanism of the changes in renal vascular tone is still not fully understood. The renin-angiotensin system behaves only passively and cannot be held responsible. Evidence is presented that changes in local adrenergic activity may determine the response of the kidney to chronic beta blockade.

Diastolic mitral regurgitation has been angiographically demonstrated in some patients with severe aortic regurgitation and/or nonobstructive cardiomyopathy. The purpose of this paper was two-fold: to study the feasibility of pulsed Doppler noninvasive detection of this unusually timed regurgitation on the basis of angiographic correlations in a group of 21 patients with such conditions and sinus rhythm with normal PR interval in 81% of the cases, and when diastolic mitral regurgitation was present, to study if it had clinical implications. Doppler detection was feasible in all cases and there were no false positive diagnoses. Comparison of haemodynamic data in patients without (group A) and with (group B) diastolic mitral regurgitation showed a significant increase in the mean values of pressures, particularly for the mean pulmonary artery and capillary wedge pressures (P less than 0.01 to 0.001), in group B. This study suggests that the recording of mitral flow velocity should be routinely performed in patients with such pathological conditions, since the finding of diastolic mitral regurgitation may have clinical significance.

The 'calcium paradox', i.e. irreversible loss of mechanical and electrical activity after a few minutes Ca2+-free perfusion and subsequent reperfusion with Ca2+-containing medium, was originally demonstrated in rat heart and later in other homoiotherms. It was absent in poikilotherms. The present paper describes the effect of Ca2+-free superfusion on human myocardium at normo- and hypothermia using isometrically mounted, stimulated strips from auricular tissue excised during cardiac surgery. The experiments (including equilibration period) were performed at 37 degrees C, 30 degrees or 25 degrees C. When Ca2+-free and EGTA-containing solution was introduced the force decline started immediately. After 10 min Ca2+-containing medium was reintroduced. Force recovery within 40 min was at 37 degrees C 16% and at 30 degrees C 28% of initial force value. Force recovery in 25 degrees C group was substantially better. Contracture which occurred when Ca2+-containing solution was reintroduced was very strong at 37 degrees C (+ 102%) and weaker at lower temperatures (30 degrees C +48% and 25 degrees C +17%). The extent of loss of mechanical activity and of contracture following the period of Ca2+-free superfusion give evidence that calcium paradox can be provoked in human myocardium and can be prevented by hypothermia.

The clinical features of the ARVD are variable. No one clinical feature is diagnostic. In this paper we will review commonly found features.

The purpose of this paper is to review the presently available information on the effect of antiarrhythmic drugs and of map-guided antitachycardia surgery on ventricular late potentials. Studies in experimental myocardial infarction have shown that antiarrhythmic drugs are able to prolong regional low-amplitude fractionated electrical activity. However, no correlation between changes in duration of low-amplitude electrical activity and antiarrhythmic drug efficacy could be demonstrated. A similar lack of correlation between changes in duration of late potentials as recorded by the signal averaging technique from the body surface and inducibility or suppression of ventricular tachycardia were observed. Neither changes in duration or amplitude nor in the frequency content of ventricular late potentials showed an unequivocal correlation with drug efficacy. By contrast, there is convincing evidence that exclusion of arrhythmogenic tissue by map-guided antitachycardia surgery correlates with the loss of late potentials postoperatively in a high percentage of cases. If, however, late potentials persist after surgery, there is a high chance of ventricular tachycardia being still inducible postoperatively. A loss of ventricular late potentials by surgery may be the result of isolation of the arrhythmogenic tissue, devitalization and/or removal. In conclusion, there is presently no convincing evidence that any of the parameters for characterization of ventricular late potentials is clinically useful to predict the efficacy of antiarrhythmic drug therapy. On the other hand, ventricular late potentials have proved useful for prediction of the success of map-guided antitachycardia surgery.

Electrode catheter ablation (fulguration) is a new technique for the treatment of ventricular tachycardia resistant to medical treatment. It proved effective in our hands in a series of 65 cases of ventricular tachycardia of varied origin. This paper reports the early results in a subgroup of 13 patients suffering from arrhythmogenic right ventricular dysplasia in whom shocks ranging from 160 to 280 J, single or multiple, in one or up to three sessions were delivered. In the 11 patients surviving the DC ablation procedure single or multiple monomorphic sustained VT was brought under control. However, four patients (36%) required therapeutic antiarrhythmic treatment following the fulguration therapy. During the learning phase one case of death was related to poor catheter selection and the other to poor protocol. The post-mortem study of the effect of shocks depends on the anatomical structure to which the shocks have been delivered.

In this paper we present the case of an 18-year old asymptomatic woman whose routine chest radiograph revealed an enlarged cardiac silhouette which was caused by a chylopericardium due to a lymphangioma of the thymus.

This paper reports a case of severe low output cardiac failure due to congestive (alcoholic) cardiomyopathy which was unresponsive to dopamine infusion, but which improved rapidly on intravenous practolol therapy. The therapeutic range of beta-blockade turned out to be quite narrow.