Objective features of the surface electrocardiogram during ventricular tachyarrhythmias

The aim of this study was to quantify the electrocardiographicsignal characteristics of three types of ventricular arrhythmia;monomorphic ventricular tachycardia, polymorphic ventriculartachycardia and ventricular fibrillation. Patients in a coronarycare unit were monitored using a single bipolar ECG lead. Thirtyepisodes of ventricular tachyarrhythmia (ten from each group)were recorded automatically by computer. Frequency analysisof ten consecutive 1 s epochs from each recording gave 100 spectrafor each tachyarrhythmia group. Each spectrum was characterisedby the frequency, width and proportional size of the dominantpeak. Despite a qualitative similarity in spectral appearance,there were significant differrences in all characteristics betweenthe tachyarrhythmia groups (P<0·025). Ventricularfibrillation had a higher mean dominant frequency (4·8Hz) than polymorphic ventricular tachycardia (3·7 Hz)and monomorphic ventricular tachycardia (3·8 Hz). Thedominant frequency of ventricular fibrillation was also morevariable than that of monomorphic ventricular tachycardia (P<0·01).Mean peak size was largest for monomorphic ventricular tachycardia(0·78) and smallest for ventricular fibrillation (0·64).The single spectral peaks seen throughout this study indicatethat all three tachyarrhythmias have an underlying periodicmechanism. The difference in spectral characteristics show thatvarying degrees of myocardial electrical organisation can bequantified from surface ECG features.     

Does in-hospital ventricular fibrillation affect prognosis after myocardial infarction?

AIM: The aim of this study was to estimate the prognostic informationto be gained from ventricular fibrillation in patients withmyocardial infarction. METHODS AND RESULTS: We studied 4259 consecutive patients with myocardial infarctionadmitted to one centre in 1977–1988. Five hundred andtwenty-eight (12·4%) of the patients had ventricularfibrillation in hospital. The following risk factors were includedin multivariate models to estimate their importance for 30-dayand long-term (median 7 year) prognosis: age, gender, ventricularfibrillation, congestive heart failure, pulmonary oedema, cardiogenicshock, other cardiac arrest and atrial fibrillation. We foundthat the odds ratio for death on days 6–30 was 6·34(3·55–11·30, 95% confidence limits, P<0·001)for patients with primary ventricular fibrillation (withoutheart failure) and 4·06 (2·68–6·14,p<0·001) for patients with ventricular fibrillationsecondary to heart failure compared to patients without ventricularfibrillation. For patients surviving more than 30 days, relativerisk of death in those with ventricular fibrillation was 1·11(95% confidence interval 0·93–1·34, P=0·26).Logistic regression analysis of relative risk associated withventricular fibrillation in time intervals, indicated that theimportance of ventricular fibrillation for risk of death wasexhausted during the initial 60 days after infarction. CONCLUSION: Ventricular fibrillation is associated with an independent increasedrisk of death within 0–60 days after infarction. Afterthis period, the prognosis in survivors of ventricular fibrillationdoes not differ significantly from patients without ventricularfibrillation.     

Factors of importance to Doppler indices of left ventricular filling in 50-year-old healthy subjects

Age is an important determinant of Doppler indices of left ventriculardiastolic filling in normal subjects. To define reference valuesand factors of importance to Doppler indices of left ventricularfilling in subjects of similar age, 58 men and 76 women aged50 years underwent Doppler echocardiography. All those takingpart in the study were healthy. When gender was analysed ina multivariate model it showed a significant independent correlationwith the peak velocity of early diastolic filling (E wave) (P<0·00l)and the early to atrial peak velocity (E/A) ratio (P<0·0l).The peak E wave velocity was 0·75±0·11m . s^–1 vs 0·66±0·10 m . s^–1(P<0·0O1) and the E/A ratio was 1·24±0·25vs 1·14±0·20 (P<0·05) in womenand men, respectively. In multivariate analyses, heart rate,diastolic blood pressure and body mass index correlated independentlywith the E/A ratio in women (P<0·00l for all), whereasin men, heart rate, diastolic blood pressure, body mass indexand left ventricular diameter correlated independently withthe E/A ratio (P<0·00l for all). Doppler measurementsof left ventricular filling in 50-year-old healthy subjectsshowed a wide variation and were significantly associated withheart rate, diastolic blood pressure, body mass index and gender.     

Sympathetic predominance of cardiac autonomic regulation in patients with left free wall accessory pathway and orthodromic atrioventricular reentrant tachycardia

AIMS: The aim of this study was to compare cardiac autonomic regulationin patients with a history of paroxysmal supraventricular tachyarrhythmias,such as atrioventricular nodal reentrant tachycardia and atrioventricularreentrant tachycardia, and healthy controls. METHODS AND RESULTS: Seventeen patients with paroxysmal atrioventricular nodal reentranttachycardia (atrioventricular nodal reentrant tachycardia group),14 patients with overt preexcitation and paroxysmal atrioventricularreentrant tachycardia caused by a left free wall accessory pathway(atrioventricular reentrant tachycardia group) and 14 healthycontrol subjects, were studied. The patients and the controlswere age and gender matched. Cardiac autonomic regulation wasassessed by means of frequency domain analysis of heart ratevariability at rest, during head-up tilt, active standing, treadmillexercise and after exercise. The high frequency component (0·15–0·5 Hz)of heart rate variability tended to be lower and the low frequencycomponent (0·04–0·15 Hz) tended to be higheramong the atrioventricular reentrant tachycardia patients thanin atrioventricular nodal reentrant tachycardia patients andcontrols. The difference reached statistical significance atrest (P<0·05) and during standing (P<0·05atrioventricular reentrant tachycardia vs atrioventricular nodalreentrant tachycardia and P<0·01 atrioventricularreentrant tachycardia vs controls). Accordingly, the low-to-highfrequency ratio — the marker of cardiac sympathetic regulation— was higher in atrioventricular reentrant tachycardiapatients than in atrioventricular nodal reentrant tachycardiapatients (P<0·05 at rest and during standing) andcontrols (P<0·01 during standing). CONCLUSION: The cardiac autonomic status in atrioventricular reentrant tachycardiapatients was suggestive of a higher sympathetic tone than inatrioventricular nodal reentrant tachycardia patients or healthycontrols. This may be related to inhomogeneous ventricular activationin the presence of antegrade conduction via the accessory atrioventricularpathway.     

Re-evaluation of the role of P-wave duration and morphology as predictors of atrial fibrillation and flutter after coronary artery bypass surgery

To evaluate the significance of P-wave duration and morphologyfor the development of post-operative atrial fibrillation/flutter,we investigated 189 consecutive patients scheduled for electivecoronary artery bypass surgery. The longest pre-operative totalP-wave duration was measured from the standard electrocardiogramat a paper speed of 50 mm. s^–1 (mean of two independentobservers). By the signal averaging technique we determinedthe pre-operative total P-wave duration, and root-mean squarevoltage of the last 10, 20, and 30 ms of the filtered (40–250Hz) P-wave from a vector composite of three orthogonal leadsat noise level 0·2 µV. Forty-two (22%) of the patientsdeveloped atrial fibrillation/flutter. Older age (mean ±SD) 62 ± 8 vs 56 ± 8 years (P<0·000),increasing body weight 83 ± 11 vs 79 ± 12kg (P=0·05),treatment for hypertension 26 vs 13% (P=0·04), and alonger P-wave duration in the standard electrocardiogram 129± 12 vs 124 ± 12 ms (P=0·01 were associatedwith development of atrial fibrillation/flutter documented bya 12-lead electrocardiogram. Logistic regression analysis identifiedindependent predictors, estimated adjusted relative risk (95%confidence interval) of atrial fibrillation/flutter: with age>60 years, the relative risk was 4·46 (2·05–9·73),and body weight >80 kg, the relative risk was 3·81(l·71–8·46). Thus, P-wave duration and morphologydid not provide significant information on the risk of atrialfibrillation/flutter when controlling for the effects of increasingage and body weight.     

The electrophysiological effects of flosequinan

We have evaluated the acute electrophysiological effects offlosequinan in 18 patients with normal ventricular function.Following intravenous infusion of flosequinan 100 mg over 1h, mean (SD) systolic blood pressure fell from 131 ±19 to 120±22mmHg (P<0·02) and there was significantshortening of sinus cycle length (732±151 to 575±93ms, P<0·001), AH interval (110±45 to 71±19ms, P<0·01) QRS duration (98±28 to 91±26ms, P<0·02) and QT interval (373±47 to 337±35ms, P<0·001 but no change in sinus node recovery time,intra-atrial conduction time, HV interval or the corrected QT_cinterval. There was a reduction in both anterograde atrioventricularWenckebach cycle length (299±53 to 259 ±52 ms,P<0·01) and retrograde ventriculoatrial Wenckebachcycle length (375 ± 77 to 300 ± 56 ms, P<0·01).There was no change in atrial or ventricular effective refractoryperiod (ERP) but atrial functional refractory period (FRP) shortened(233 ± 31 to 212 ± 24 ms, P=007) as did ventricularFRP (249 ± 24 to 234 ± 21 ms, P<0·01).Patients received an oral dose of flosequinan 50 mg 12 h later.By 24 h, sinus cycle length, QRS duration and the QT intervalhad all returned towards baseline values, but ventricular ERPhad lengthened (199±22 to 215±26 ms, P<0·06).Programmed ventricular stimulation did not result in any sustainedarrhythmias before or after flosequinan. The observed electrophysiologicaleffects of flosequinan infusion are consistent with reflex sympatheticactivation. There was no conclusive evidence for any directelectrophysiological effect or for contraction-excitation feedback.No proarrhythmic effects were observed.     

The electrophysiological effects of flosequinan

We have evaluated the acute electrophysiological effects offlosequinan in 18 patients with normal ventricular function.Following intravenous infusion of flosequinan 100 mg over 1h, mean (SD) systolic blood pressure fell from 131 ±19 to 120±22mmHg (P<0·02) and there was significantshortening of sinus cycle length (732±151 to 575±93ms, P<0·001), AH interval (110±45 to 71±19ms, P<0·01) QRS duration (98±28 to 91±26ms, P<0·02) and QT interval (373±47 to 337±35ms, P<0·001 but no change in sinus node recovery time,intra-atrial conduction time, HV interval or the corrected QT_cinterval. There was a reduction in both anterograde atrioventricularWenckebach cycle length (299±53 to 259 ±52 ms,P<0·01) and retrograde ventriculoatrial Wenckebachcycle length (375 ± 77 to 300 ± 56 ms, P<0·01).There was no change in atrial or ventricular effective refractoryperiod (ERP) but atrial functional refractory period (FRP) shortened(233 ± 31 to 212 ± 24 ms, P=007) as did ventricularFRP (249 ± 24 to 234 ± 21 ms, P<0·01).Patients received an oral dose of flosequinan 50 mg 12 h later.By 24 h, sinus cycle length, QRS duration and the QT intervalhad all returned towards baseline values, but ventricular ERPhad lengthened (199±22 to 215±26 ms, P<0·06).Programmed ventricular stimulation did not result in any sustainedarrhythmias before or after flosequinan. The observed electrophysiologicaleffects of flosequinan infusion are consistent with reflex sympatheticactivation. There was no conclusive evidence for any directelectrophysiological effect or for contraction-excitation feedback.No proarrhythmic effects were observed.     

Effects of respiration on left ventricular diastolic function in healthy children

Pulsed Doppler echocardiographic indices of mitral valve fillingwere measured in 20 healthy children, between 3 and 125 yearsold, in order to evaluate the effects of spontaneous respirationon left ventricular diastolic filling patterns. There were significantrespiratory variations in four parameters of left ventriculardiastolic function: The peak early filling velocity, the ratioof early to late peak filling velocity, and the ratio of earlyto late diastolic velocity-time integral decreased significantlyduring inspiration (mean decrease 7%, P<0·05; 16%,P<0·01; and 12%, P<0·05, respectively).On the other hand there was a significant increase in late peakfilling velocity with inspiration (10% increase, P<0·05).Other variables of left ventricular diastolic filling were unchangedwith inspiration. These results suggest that assessment of leftventricular diastolic function in children should be standardizedwith regard to respiratory phases in any clinical application. (Eur Heart J 1996; 17: 453%456)     

Alteration of peripheral vasodilatory reserve capacity after cardioversion of atrial fibrillation

In atrial fibrillation, exercise capacity is often reduced.This is usually ascribed to a decreased cardiac output as comparedwith sinus rhythm. Very few studies, however, have focused onchanges in the peripheral blood flow during atrial fibrillationas a potential mechanism for exercise limitation. The aim ofthe present study was to determine the effect of conversionof atrial fibrillation to sinus rhythm on peripheral blood flow. Calf blood flow, using an electrocardiogram-triggered venousocclusion plethysmograph, and peak oxygen consumption (peakVO₂), using treadmill exercise testing, were studied in 28 patientswith chronic atrial fibrillation eligible for electrical cardioversion.Measurements were performed before cardioversion, and repeated1 day and 1 month thereafter. Calf blood flow at rest, maximalcalf blood flow, and minimal calf vascular resistance duringthe hyperaemic response immediately following 700 J of calfexercise were determined plethysmographically. One day and 1 month after cardioversion, 23 and 14 patientswere still in sinus rhythm, respectively. In patients who stillhad sinus rhythm after 1 month, maximal calf blood flow increasedfrom 33·7±12 to 40·0±13 ml. 100ml ^{–1 min –1} (P<0.01) and minimal calf vascularresistance fell from 3·2±0·9 to 2·7±0·7mmHg.ml^–1. 100 ml^–1. min^–1 (P<0·01);peak VO₂ increased from 21·3±4 to 24·2±5ml. min^–1. kg^–1 (P<0·001). Calf bloodflow at rest did not improve. In contrast, no significant changesin maximal calf blood flow, minimal calf vascular resistanceand peak VO₂ occurred in patients who had atrial fibrillation1 month after cardioversion. A significant correlation was foundbetween changes in maximal calf blood flow and peak VO₂ 1 monthafter cardioversion (r=0·53, P<0·01). One dayafter cardioversion, no changes in calf blood flow or peak VO₂,were found, either in patients with sinus rhythm or atrial fibrillation. In conclusion, transition from chronic atrial fibrillation tosinus rhythm is associated with a (delayed) improvement in maximalcalf blood flow, minimal calf vascular resistance, and peakVO₂. Our findings suggest that increase in vasodilatory reserve capacitymay contribute to the improvement of exercise capacity aftercardioversion of atrial fibrillation.     

Echocardiographic assessment of myocardial performance after prolonged strenuous exercise

To determine the effect of strenuous prolonged exercise on systolicand diastolic left ventricular function, 11 non-elite marathonrunners aged 37±7 years (mean±SD) were studiedbefore and during early recovery from a marathon race. Cavitydimensions, wall thickness, and fractional shortening were computedfrom two-dimensionally guided M-mode echocardiograms. Dopplerleft ventricular inflow tract recordings were analysed for peakearly and late velocities and their ratio. In seven subjects,heart frequency was recorded throughout the race. These subjectsran the marathon at 87±4% of their maximal heart rate.Left ventricular diastolic dimension was slightly reduced atthe end of the race (49·4±4·2 mm to 47·3±5·1mm:P<0·05). Fractional shortening remained unchanged,although blood pressure (P<0·001) and systolic itall stress (P<0·01) were decreased. The left ventricularfilling pattern was unchanged, and the ratio of early to latevelocities remained constant. These results suggest that thefractional shortening was a result of the opposing effects ofchanges in preload and afterload. However, the absence of achange in the end systolic dimension, despite a marked reductionin afterload and the occurrence of septal akinesia in one subjectafter the race could only suggest that strenuous prolonged exercisemay alter mnyocardial performance.     

The effect of meals of differing composition on exercise tolerance in patients with angina pectoris

In this study we compared different dietary constituents andtheir effect on the angina threshold. We compared carbohydrate-rich,fat-rich and balanced liquid diets on effort tolerance in 14patients of mean (range) 61 (41–73) years of age withchronic stable angina. On four different occasions at least1 week apart, patients had exercise treadmill tests after anovernight fast and then after a rest period of I h ingestedone of three different approximately isocalorific (about 4000kJ) liquid drinks of 600 ml consisting mainly of: fat, carbohydrateor a balanced meal with an equal volume of water as control.Meals were given in random order. Analysis of the mean (SD) differences in heart rate betweenfasting and the post-prandial state for the different mealsrevealed a significant increase between water and the othermeals, fat (+4(6) beats.min^–1 P<0·002), balanced(+9(17) beats. min^–1 P<0·004), and carbohydrate(+ 10(12) beats . min ^–1 P<0·002) There wasno significant difference between the groups as regards systolicor diastolic blood pressure. Cardiac output increased followingthe meals but decreased after water; however, there was a significantdifference between water and balanced meals. Exercise tolerancefell following all the meals but was significantly greater aftera balanced (mean (SD) – 108(129) s P<0·001)and carbohydrate meal (– 92(52) s P<0·001).The reduction in exercise duration following a fat meal (–36(53) s) was not significantly different from that followingwater (– 8(43) s) but was significantly smaller than aftera carbohydrate meal (P<0·02). Time to I mm of ST depressionshowed similar changes to that of total exercise duration, beingsignificantly lower after a carbohydrate (mean (SD) –76(77) s P<0·01) and balanced meal (– 76(63)s P<0·0005). Time to 1 mm ST depression, althoughreduced by a fat meal (– 15(84) s) was significantly lessthan after a carbohydrate meal (P<0·02). In conclusion, patients with chronic stable angina have impairedeffort tolerance and a lower angina threshold after high caloriecontaining liquid meals. Meals rich in carbohydrate have greatereffects than meals where the majority of calories are derivedfrom fat. Patients should be advised to avoid exercise in thefirst 30 mm after eating. (Eur Heart J 1996; 17: 394–398)     

Impact of dietary sodium intake on left ventricular diastolic filling in early essential hypertension

Aims Dietary sodium intake modulates left ventricular hypertrophyin established essential hypertension independent of blood pressurelevel. We conducted this study to elucidate the relationshipbetween sodium intake and left ventricular structural or functionalchanges in early essential hypertension. Methods Forty-four young male patients (age 25·9±2·6years) with mild essential hypertension that had never beentreated and 45 normotensive male control subjects of similarage were examined. Dietary sodium intake was measured from 24hurinary sodium excretion, blood pressure from 24h ambulatorymonitoring (SpaceLabs 90207), left ventricular structure from2-D guided M-mode echocardiography, and diastolic filling ofthe left ventricle (as the main compound of diastolic functionin a young population) by pulse-wave Doppler sonography. Results In hypertensive patients, daily sodium excretion correlatedwith the ratio of late (A) to early (E) maximum velocity (VmaxA/E; r=+0·27,P=0·07), velocity time integrals(A/E; r=+0·54,P<0·001) as well as atrial contribution,as a percent of left ventricular filling (VH ATCO; r=+0·52,P<0·001)independent of heart rate, whereas the opposite correlationswere observed in normotensives (allP<0·001). Stepwisemultiple regression analysis confirmed these results. Sodiumexcretion emerged as the strongest independent determinant ofimpaired diastolic filling in hypertensive patients (velocitytime integrals A/E: R²=0·49, ß=+0·57,P=0·0001;VH ATCO: R²=0·48, ß=+0·56,P<0·0001;Vmax A/E: ns). In normotensive subjects, sodium excretion wasa similar strong, but inverse deter-minant of diastolic filling(velocity time integrals A/E: R²=0·40, ß=–0·43,P=0·0028).Heart rate was a strong determinant of diastolic filling inhypertensive patients (ß=+0·55,P=0·0002)and in normotensive subjects (ß=+0·34,P=0·011).Left ventricular mass and end-diastolic volume index were notrelated to diastolic filling in either group. Conclusion In early essential hypertension, sodium excretion is correlatedwith impaired left ventricular diastolic filling independentof left ventricular mass. The renin-angiotensin-aldosteronesystem might be a mediator of the observed correlation.     

Impact of the implantable cardioverter-defibrillator on rehospitalizations

Patients who survive out-of-hospital ventricular tachycardiaor ventricular fibrillation are at risk of sudden cardiac deathand often return to hospital after initial discharge. The frequencyand duration of readmittance to hospital are not well known.Thus, the purpose of this study was to evaluate the impact ofthe implantable cardioverter defibrillator on frequency andduration of hospitalizations. METHODS: Between 1989 and 1993, 38 consecutive patients who had drug-refractoryventricular tachyarrhythmias were selected for the study. Atotal of 38 patients were implanted with the implantable cardioverter-defibrillatorin accordance with the guidelines of the European Society ofCardiology. This analysis includes 35 of the 38 patients (92%).All hospitalizations which occurred one year before and oneyear after were studied. Clinical information for all patientswas obtained by consulting medical records and by interviewingpersonal general practitioners. RESULTS: The annual number of hospitalizations before and after implantationof the implantable cardioverter defibrillator was, respectively,3·28 ± 2 hospitalizations/patient/year and 0·88± 1·23 hospitalizations/patient/year (P<0·05).Before implantation of the implantable cardioverter-defibrillator,patients were hospitalized a mean of 32·94 plusmn; 24·18days/patient/year and after, 9·31 ± 32·14days/patient/year (P<0·05). The number of hospitalizationsfor cardiac reasons decreased by 90%. Before implantation, themost frequent cause was ventricular tachyarrhythmia (47 hospitalizationsfor ventricular tachycardia and eight for ventricular fibrillation),while after implantation, it was as a result of the shock fromthe implantable cardioverter defibrillator (II hospitalizations).The number of hospitalizations for non-cardiac reasons weresimilar in the two time periods. Of the 35 patients, 26 (74%)had at least one appropriate successful ventricular tachycardiainterrupted by the implantable cardioverter-defibrillator, while17 patients (49%) had their ventricular fibrillation terminated.There is a significant difference in the rate of hospitalizationsto intensive care units (ICU) between the two periods. Beforeimplantation, 30% of hospital days were spent in the ICU, with3% after. CONCLUSIONS: This study documents that the implantable cardioverter-defibrillatornot only reduces the frequency and duration of hospital stays,but reduces admissions to the more expensive units in hospital.Taking into account the reduction in hospitalizations, the paybackperiod for the implantation of an implantable cardioverter-defibrillatoris 19 months. (Eur Heart J 1996; 17: 1565–1571)     

Diagnostic accuracy of dobutamine stress echocardiography for detection of coronary heart disease in hypertensive patients

To compare the diagnostic accuracy between dobutamme echocardiographyand treadmill exercise electrocardiography in detecting coronaryartery disease in hypertensive patients, 43 patients withoutelectrocardiographic evidence of left ventricular hypertrophyand basal ST-T changes, who had also undergone coronary angiography,were further evaluated by dobutamine echocardiography. The patientsalso underwent treadmill exercise echocardiography. Left ventricularmass index was calculated by echocardiography. Twenty-nine patientshad coronary artery disease, of whom 22 had multi-vessel diseaseand 14 a normal coronary anatomy. Twenty-eight patients hadan increased left ventricular mass index. The sensitivitiesof dobutaniine echocardiography and exercise electrocardiographyfor detecting coronary artery disease were 93% and 72% (P=0·08)respectively, and the specificities were 100% and 29%(P<0·005),respectively. Logistic regression analysis showed exercise electrocardiographyto be a poor predictor of coronary artery disease (P<0·09)but dobutamine echocardiography was significantly better (P<0·00l).When patients with increased left ventricular mass index wereexcluded, prediction of coronary anatomy by exercise electrocardiographyimproved only marginally (P=0·4) while dobutamine echocardiographywas significantly better (P<0·00l). Thus dobutamineechocardiography is superior to exercise electrocardiographyfor diagnosis of coronary artery disease in hypertensive patients.     

The influence of muscle mass, strength, fatigability and blood flow on exercise capacity in cachectic and non-cachectic patients with chronic heart failure

BACKGROUND: The influence of age, skeletal muscle function and peripheralblood flow on exercise capacity in chronic heart failure patientsis controversial, possibly due to variations in skeletal muscleatrophy. METHODS AND RESULTS: To assess predictors of exercise capacity in patients with clinicalcardiac cachexia, we studied 16 cachectic and 39 non-cachecticmale chronic heart failure patients of similar age and ejectionfraction. All cachectic patients were wasted (% ideal body weight:81 1·9 vs 105·2±2·1, P<0·mean±SEM) and had documented weight loss (5–30kg). Peak oxygen consumption (14·9±1·4vs 16·3±0·6 ml.kg^–1, min ^–1,resting, and peak blood flow (plethysmography) and 20 min fatigability(% baseline strength) were all similar between the two groups.Quadriceps strength, muscle size (all P<0·0001), strengthper unit muscle (right: P<0·05; left: P<0·0·01)and 5 min fatigability (P<0·05) were all lower incachectic patients. In non-cachectic patients, age (R=0·48and quadriceps strength (R=0·43, all P<0·01)predicted peak oxygen consumption. Only in cachectic patientsdid peak blood flow predict peak oxygen consumption significantly(R=0·72, P0·005), whereas age and strength didnot. Similar findings were confirmed using other previouslypublished definitions of cardiac cachexia. CONCLUSION: The predictors of exercise capacity change with the developmentof cardiac cachexia from age and strength to peak blood flow.This shift may be caused by additional endocrine or catabolicabnormalities active in end stage heart failure.     

Left ventricular function after repeated episodes of ventricular fibrillation and defibrillation assessed by transoesophageal echocardiography

Background Investigators studying the effects of cardioverter-defibrillatorson left ventricular systolic function have given only minorattention to the diastolic effects. Objectives The purpose of this study was to investigate theimpact of repeated episodes of ventricular fibrillation anddefibrillation on systolic function and diastolic filling ofthe left ventricle during non-thoracotomy implantation of acardioverter-defibrillator. Methods Systolic function and diastolic filling of the leftventricle were assessed peri-operatively on a beat-by-beat basisusing a transoesophageal echo-Doppler technique in 12 patientsduring 4 episodes of ventricular fibrillation and defibrillation.Systolic function was assessed from the fractional area changeand diastolic filling from the E/A ratio. Arterial blood pressureand the ECG were recorded continuously. Results Blood pressure and heart rate did not change significantlythroughout the procedure. The systolic function, similarly,was not significantly affected; the only changes were seen inthe first two beats after defibrillation when the mean fractionalarea increased from 0·2±0·01 to 0·4±0·02and 0·3±0·02, respectively (P<0·001).Diastolic filling was, however, impaired as reflected by a decreasein the E/A ratio from 2·6±0·5 before to1·6±0·4 (P<0·01) after repeatedthreshold tests. Conclusions. While the combined ischaemic and electrical traumacaused by repeated episodes of ventricular fibrillation anddefibrillation during the implantation of a cardioverter-defibrillatordid not cause any systolic dysfunction, diastolic filling wassignificantly impaired.     

Acute effects of balloon valvuloplasty and pacing on left ventricular performance in children with moderate pulmonary valve stenosis, analysed by systolic and diastolic pressure--volume relationships

Right ventricular overload of volume and/or pressure type mayaffect left ventricular systolic and diastolic function. Thishas been shown in animal studies and has been suggested in non-invasivestudies in man. Altered geometry of the left ventricle, myocardialhypertrophy and changes in contractile state may be responsiblefor the change in function. Balloon valvuloplasty is an effectivetreatment for isolated valvular pulmonary stenosis in children,and results in an immediate decrease of right ventricular systolicpressure. Whether this results in immediate changes in leftventricular performance is unknown. Eight children (age 5·2to 13·9 years) with moderate pulmonary valve stenosisunderwent pulmonary balloon valvuloplasty under general anaesthesia.Left ventricular function measurements before and after valvuloplastywere performed using a combined micromanometer-conductance catheterto obtain end-systolic (ESPVR) and end-diastolic (EDPVR) pressure-volumerelationships employing inferior vena cava occlusion both atnormal and pacing-induced increased heart rates. Pulmonary valvuloplasty resulted in a decrease in peak systolicright ventricular pressure from 62·8±13·5to 34·4 ± 7·3 mmHg (P<0·001),without significant changes in left ventricular systolic andend-diastolic pressure, or in cardiac index. The ESPVR was fittedto a linear function to obtain the slope (E_es and the volumeintercept at 75 mmHg (V₇₅ The EDPVR was fitted to an exponentialfunction. At baseline, E_es was 1·68±0·99mmHg. ml^–1 and V₇₅ was 33·6 ± 21·8ml. Neither valvuloplasty nor pacing, which increased mean heartrate from 81 to 112 beats. min^–1 (P<0·001) resultedin significant changes of the parameters E_es, or V₇₅ The EDPVRwas not affected by valvuloplasty either, but pacing resultedin a change of its stiffness constant from 0·042 ±0·019 to 0·034 ± 0·018 mmHg . ml^–1(P<0·05) and pressure intercept from 0·97±0·51to 1·37±0·86 mmHg (P<0·05). Theeffect of pacing on left ventricular function before and aftervalvuloplasty was comparable. Neither balloon dilatation for moderate valvular pulmonary slenosis,nor pacing within the physiological range results in immediatechanges in left ventricular contractile performance in children.     

Effects of captopril on ventricular arrhythmias in the early and late phase of suspected acute myocardial infarction: Randomized, placebo-controlled substudy of ISIS-4

The antiarrhythmic effect of oral captopril was studied duringthe early (day 3) and late (day 14) phase of acute myocardialinfarction among 304 patients in a randomized placebo-controlledsubstudy of ISIS-4. Ventricular arrhythmias (ventricular ectopic beats per hour)occurred significantly less frequently among captopril-allocatedpatients than among those allocated placebo at day 3 (logarithmicscale: 0·48 ± 0·8 captopril vs 0·84± 1·3 placebo; P<0·003) and at day 14(0·51 ± 1·0 vs 0·77 ± 1·3;P<0·05). The number of patients with frequent ventriculararrhythmias (more than 10 ventricular ectopic beats per hour)was also significantly lower among those allocated captoprilat day 3 (7·3% vs 14·4% P<0·05) andat day 14 (7·3% vs 14·8%; P<0·05). These results support the hypothesis that the activation ofthe renin-angiotensin-aldosterone and sympathetic system mayunderlie heart rhythm disturbances in acute myocardial infarction,and that early use of converting enzyme inhibitor therapy mayameliorate these disturbances. (Eur Heart J 1996; 17: 1506–1510)     

Clinical cardiac electrophysiologic evaluation of the positive inotropic agent, DPI 201-106

DPI 201–106 is a new positive inotropic agent. The cardiacelectrophysiology of 16 patients was studied before and duringDPI 201–106 administration (loading dose of intravenousDPI 201–106, 1·8 mg kg^–1 h^–1 administeredover 10 min, followed by a maintenance dose of 0·2 mgkg^–1 h^–1). DPI 201–106 had no effect on thesinus node. The AH interval during fixed-rate atrial pacingbecame prolonged during DPI 201–106 infusion. There wasa significant prolongation of the QT interval [QT (corrected),417 ± 22 to 502 ± 35 ms, P<0·05; QT(atrial pacing at 600 ms), 374 ±17 to 419 ± 23ms, P<0·05; QT (ventricular pacing at 600 ms), 409± 37 to 449 ± 30 ms, P<0·05]. The ventriculareffective refractory period significantly prolonged during DPI201–106 administration (242 ± 21 to 287 ±56 ms, P < 0·05), but the supernormal-period durationdecreased. The atrial effective refractory period was shortenedin four patients and prolonged in one (261 ± 67 to 240± 53 ms, NS). The corrected atrial repolarization time(PT_ac) shortened significantly during DPI 210–106 infusion(479 ± 26 to 445 ± 22 ms at 20 min of the maintenancedose, P<0·05). Atrial fibrillation was initiated infive patients during DPI infusion, but no ventricular arrhythmiawas provoked. These findings suggest that DPI 201–106has novel differential electrophysiological effects on atriaand ventricles.     

QT dispersion and RR variations on 12-lead ECGs in patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy

Increased QT dispersion, which has been proposed as a markerof ventricular repolarization inhomogeneity, may predisposeto ventricular arrhythmias. Data on QT disper sion in patientswith congestive heart failure are scarce. In this study, conventional12-lead ECGs were recorded in 135 consecutive patients withcongestive heart failure secondary to idiopathic dilated cardiomyopathy.Seventy-five patients were excluded from QT interval assessmentsdue to one or more of the following reasons: (1) low amplitudeof the T wave (n=3), (2) atrial fibrillation (n=26) and (3)bundle branch block (n=46). QT dispersion was calculated as(I) QT-range: the difference between the maximum and minimumQT intervals on any of the 12 leads and (2) QT-SD: the standarddeviation of the QT interval in all the 12 leads. RR intervalswere measured in leads II, aVL, V₂ and V₅ QT-SD (20·85± 5·00 ms) was significantly (r=0·8997,P<0·00l) related to QT-range (6565 ± l5 ms),but not to the QT interval. Neither QT-range nor QT-SD was significantlyrelated to age, left ventricular dimensions, left ventricularend diastolic pressure, left ventricular ejection fraction orleft ventricular wall thickness. There was no significant differencein QT dispersion between survivors and those who died (n=8)or were transplanted (n=9) during 34 ± 23 month follow-up.No significant difference in QT dispersion was observed betweenpatients with and without ventricular tachycardia ( three consecutivebeats) detected on 24-h Holter ECGs. RR interval variation wassignificantly lower in patients who died compared with survivors(standard deviation: 10·37 ± 3·61 vs 36·02± 35·03 ms, P<0·001; coefficient ofvariance: 1·87 ± 0·7 vs 4·50 ±4·9%, P=0 This was also true in patients with bundlebranch block. These observations suggest that QT dispersionin idiopathic dilated cardiomyopathy is not significantly relatedto either QT interval or cardiac size and function and doesnot predict death. The application of QT dispersion assessmentis limited by the commonly encountered atrial fibrillation andbundle branch block in this patient population. However, reducedRR variation on standard 12-lead ECGs has important prognosticimplications in these patients.