Influence of left ventricular filling profile during preceding control beats on the occurrence of pulse deficit caused by ventricular premature contractions

This study was designed to investigate whether the left ventricularfilling profile during preceding control beats significantlyaffects the pulse deficit caused by ventricular premature contractions(VPCs). The study group consisted of 18 patients (10 men, eightwomen, 15–85 years old) who underwent electrophysiologicalcatheterization because of sinus bradycardia. Using a temporarypacing lead inserted in the right ventricular apex, isolatedVPCs with various coupling intervals were produced by electricalstimulation of the right ventricle. During the production ofthe VPCs, the mitral filling flow velocity using pulsed waveDoppler echocardiography, the femoral arterial pressure curveand the electrocardiogram were simultaneously recorded. Theright ventricle was siimulated 800, 750, 700, 650, 600, 550,500, 450 and 400 ms after the triggered control beat QRS complex.Pulse pressures during VPCs gradually decreased in relationto the shortening of the extra-systolic beat coupling interval.The longest coupling interval for each subject, which causedcomplete abolition of the pressure pulse during the VPC, wasdefined as the pulse deficit coupling interval. The early tolate diastolic velocity–time integral ratio (E_i/A_i ratio)of the mitral filling flow velocity during the control beatswhich precede the VPC was obtained as an index expressing theleft ventricular filling profile. The E_i/A_i ratio of the mitralfilling flow velocity ranged from 0.7 to 4.5 (1.8 ± 1.0).The pulse deficit coupling interval ranged from 440 to 640 ms(510 ± 60 ms). A significant negative correlation wasobserved between the E_i/A_i ratio and the pulse deficit couplinginterval (r = –0.69, P<0.01). A significant positivecorrelation was also observed between the age and the pulsedeficit coupling interval (r = 0.63, P<0.01). The findingsare consistent with the concept that pulse deficit by VPCs mayeasily occur in patients with reduced left ventricular fillingduring the early diastole.     

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.     

Left ventricular blood flow dynamics caused by ventricular premature contraction: pulsed Doppler echocardiographic study

Cardiac function at the time of ventricular premature contractions (VPC) is influenced by the coupling interval or the site of those origin. Clinical and experimental studies of the effects of VPC on intracardiac pressure dynamics have been performed; however, little is known about left ventricular blood flow dynamics. This study was attempted to determine the characteristics of blood flow dynamics in respect to the site of origin of VPC using pulsed Doppler echocardiography. The subjects consisted of 18 cases with VPC but without apparent organic heart disease. Seven cases had VPCs with a left bundle branch block pattern suggesting possible origin in the right ventricle. The other 11 cases had VPCs with a right bundle branch block pattern indicating the left ventricular origin. With the probe in the apical position, the blood flow patterns of the left ventricular outflow, central and inflow tracts were examined. The results were as follows; 1. Except for one case with shortened coupling interval, all six cases with VPCs originated from the right ventricle showed preservation of left ventricular ejection flow. 2. In two of the three cases with VPC which originated from the left ventricle and with left axis deviation, systolic flow in the left ventricular central area showed "back flow" to the apex. Ejection flow at the outflow tract was markedly diminished or disappeared in all three cases. 3. In all eight cases with VPC which originated from the left ventricle and with right axis deviation, ejection flow was slightly disturbed both in the left ventricular outflow and in the central area. 4. Ejection flow volume assessed by velocity integral indicated similar dynamics as did the ejection flow velocity. 5. In left ventriculography, asynchrony due to dyskinetic motion of the anteroapical wall was observed at the times of VPCs with left axis deviation. In conclusion, the patterns of left ventricular ejection flow dynamics depend on the site of origin of VPCs. This disturbed flow is more apparent in VPCs originating from the left ventricle compared to the right ventricle. This is especially true in cases with left axis deviation, in which VPCs arise from the posterior site of the left ventricle.     

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.     

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.     

Gender and the relationship between ventricular repolarization and cardiac cycle length during 24-h Holter recordings

AIMS: There are gender-related differences in the QT interval measuredfrom standard ECG tracings. However, these observations arebased on a limited number of beats recorded in resting conditions.Computerized Holter techniques enable ventricular repolarizationand its relationship with cardiac cycle length to be analysedlong term. Previous studies used only the initial portion ofthe QT interval to the T wave apex (QTa) to measure ventricularrepolarization; however, QTa may underestimate the total QTduration (QTe). The aims of this study were to verify whetherQTa and QTe had similar rate-dependence in normal subjects andwhether gender-related QTc differences observed in the restingECG were also present in the long-term QT interval-cycle lengthrelationship. METHODS AND RESULTS: Twenty-four hour Holter recordings were obtained in 40 healthyyoung subjects, 20 females and 20 males (mean age 28±9and 26±5 years, respectively ns). Two-channel ECG digitizedsignals were processed using new automatic QT analysis software(Ela Medical), which converted the 24-h recordings into 288030-s templates. It also measured the QT apex (QTa) QT end (QTe)and the RR interval (ms) of each template, and computed theslopes of the linear regressions of QTe and QTa values plottedagainst the corresponding RR interval (QTe/RR and QTa/RR). Femaleshad a shorter RR interval than males (803±129 vs 877±86ms, p=0·037), with longer mean QTc (420±17 vs400±200 ms, p=0·0005). In both genders, QTa/RRslopes were steeper than QTe/RR slopes (p=0·0001). BothQTa7sol;RR and QTe/RR slopes were steeper in females than inmales (QTa/RR 0·20±0·04 vs 0·16±0·03,p=0·001; QTe/RR 0·16±0·04 vs 0·13±0·03,p=0·027). Of note, QTa and QTe at fixed long cycle lengths(1000 ms) were longer in women than in men (QTa₁₀₀₀ 330±20vs 309±18 ms; p=0·002; QTe₁₀₀₀ 410±17 vs389±19 ms; p=0·002), while they did not differat fixed short cycle lengths (600 ms). CONCLUSIONS: This study demonstrates that both the initial portion of theQT interval (QTa) and the entire QT interval (QTe) are usefulsince QTa is more prolonged than QTe at increasing cycle lengths,and thus includes most of the heart rate dependency of ventricularrepolarization. In normal subjects, both the QTc and the long-termrelationship between ventricular repolarization and heart rateare affected by gender. The differences in QTa and QTe durationbetween males and females are more marked at long cycle lengthsand disappear at short cycle lengths. Finally, this study alsoproves the clinical feasibility of assessing the long-term relationshipbetween ventricular repolarization and heart rate by utilizingthe automatic measurement of the QT interval from 24-h Holterrecordings.     

Are the first repetitive reentrant VPCs a trigger or an initiation of reentrant circuit for VPCs?: Evaluation by Holter ECG in patients with reentrant sustained ventricular tachycardia]

To evaluate whether the first repetitive reentrant VPCs are a trigger or an initiation of a reentrant circuit for VPCs, we studied Holter ECGs in 13 patients with sustained ventricular tachycardia, the morphology of reentrant VPCs, the relationship between the coupling interval (N-V) and the first ventricular cycle length (V-V), and the relationship of the coupling interval (N-V) between single VPC and repetitive VPCs. In 7 patients who showed episodes of repetitive VPCs more than twice on one recording of Holter ECG, most of VPCs in the first and second beats were the same in shape (1195 out of 1466 episodes, 82%). No obvious relationship between the coupling interval (N-V) and the first ventricular cycle length (V-V) was found in 5 patients, whereas a weak inverse relationship (r = 0.32) was found in one patient, and a weak positive relationship (r = 0.38) was found in another patient. In addition, the coupling interval in repetitive VPCs was longer than that in single VPCs in 4 out of 7 patients. These results imply that, in most cases, the first VPC is the expression of initiation of a reentrant circuit for repetitive reentrant VPCs developing spontaneously.     

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.     

Left ventricle filling abnormalities prior to and following treatment of thyrotoxicosis -- is diastolic dysfunction implicated in thyrotoxic cardiomyopathy?

Despite cardiac failure being a well recognised complicationofthyrotoxicosis, systolic function has generally been reportedas maintained or enhanced. In this study, left ventricular diastolicfunction was assessed in 16 thyrotoxic patients and 18 age-matchedcontrols by pulsed-Doppler echocardiography. Patients were re-studiedafter 3 and 12 months of treatment. Prior to treatment all standardDoppler-;derived indices of diastolic function were significantlydifferent to control (isovolumic relaxation time (IVRT) 63±18.9vs 84.0±14.8 ms, peak early filling velocity (E_max) 79.2±15.2vs 61.9±10.7 cm . s^–1, peak atrial filling velocity(A_max) 68.2±17.9 vs42.2±9.4 cm . s^–1, decelerationof early filling (E/F slope) 6.1±1.8 vs3.7±1.1m . s^–1, thyrotoxic vs control). However, these fillingabnormalities appear likely to reflect the tachycardia and reducedsystemic vascular resistance (SVR) found in the patients (heartrate 102±15 vs 76 ± 9, SVR 874 ± 207 vs1293 ± 362 dynes .s^–1. cm^–5, both P<0.001).After 3 months of treatment haemodynamics were similar in thetwo groups but filling remained abnormal in patients with apattern suggesting increased transmitral pressure gradients(E_max 73.1 ± 15.1 cm.s^–1, A_max 55.8 ± 19.2cm.s^–1,E/F slope 4.9 ± 2.0m . s^–1, all P<0.05 comparedto controls). After 12 months of treatment most parameters hadreturned to normal but the atrial contribution to left ventricularfilling remained high (A_max54.7 ± 13.9 vs control 42.2± 9.4 cm . s^–1 .flow velocity integral of atrialfilling 4.7 ± 1.3 vs 3.6±11 control, both P0.01).Left ventricular filling is therefore highly abnormal beforeand during the treatment ofthyrotoxicosis. However, these changesappear unlikely to reflect an intrinsic thyrotoxic cardiomyopathyand are more likely to represent a combination of prolongedincreases in left ventricular filling pressures along with abnormalitiesof left atrial function. The abnormal Doppler parameters emphasisethe importance of sinus rhythm in maintaining left ventricularfilling in thyrotoxicosis and may explain why marked haemodynamicdeterioration may result from the development of atrial fibrillationin these patients.     

Heart failure: Effects of beta receptor antagonists on left ventricular function in patients with clinical evidence of heart failure after myocardial infarction. A double-blind comparison of metoprolol and xamoterol Echocardiographic results from the Metoprolol and Xamoterol Infarction Study (MEXIS)

Two hundred and ten patients with clinical evidence of heartfailure, developing after an acute myocardial infarction, wererandomized to treatment with the ß₁ antagonist metoprolol50–100mg b.i.d. (n=106) or the ß₁ partial agonistxamoterol 100–200 mg bid. (n=104). Left ventricular systolicand diastolic function were assessed with echocardiography andtransmitral Doppler cardiography before and after 3 and 12 monthsof double-blind treatment. E-point septal separation and percent left ventricular fractional shortening were used as indicesof systolic function. The ratio between peak early and latemitral diastolic flow (E/A ratio) and isovolumic relaxationtime were used as indices of diastolic function. In the xamoterol group, there was a deterioration in E-pointseptal separation (P<0·05). A difference between thetreatment groups was present both at 3 months (E-point septalseparation 11·4 vs 13·0 mm, P<0·0l,fractional short ening 271 vs 252%, P<005) and 12 months(E-point septal separation Ill vs 13·2 mm, P<0·05fractional shortening 26·9 vs 25·0%, P<0·05).E/A ratio increased in the metoprolol group (P<0·05)but not in the xamoterol group. At 3 months there was a significantdifference (0·85 vs 0·67, P<0·005 betweenthe groups but not at 12 months. In comparison with the ß₁-receptor antagonist metoprolol,the ß₁ partial agonist xamoterol impaired left ventricularsystolic function in patients with clinical evidence of heartfailure after an acute myocardial infarction.     

Relation of ventricular premature complexes to heart failure (from the Atherosclerosis Risk In Communities [ARIC] Study)

Analogous to rapid ventricular pacing, frequent ventricular premature complexes (VPCs) can predispose over time to cardiomyopathy and subsequent heart failure (HF). We examined the association of frequent VPCs with HF incidence in a population-based cohort, free of HF and coronary heart disease at baseline. At study baseline (1987 to 1989), ≥1 VPC on a 2-minute rhythm electrocardiographic strip was seen in 5.5% (739 of 13,486) of the middle-age (45 to 64 years old at baseline) white and black, men and women of the Atherosclerosis Risk In Communities cohort. Incident HF was defined as the first appearance of International Classification of Diseases code 428.x in the hospital discharge record or death certificate through 2005. During an average follow-up of 15.6 years, incident HF was seen in 10% the participants (19.4% of those with VPCs vs 9.4% of those without). The age-, race-, and gender-adjusted hazard ratio of HF for VPCs was 1.89 (95% confidence interval 1.59 to 2.24). After multivariable adjustment for potential confounders, the hazard ratio of HF for those with any VPC versus no VPC was 1.63 (95% confidence interval 1.36 to 1.96). After additional adjustment for incident coronary heart disease as a time-varying covariate, the hazard ratio was 1.71 (95% confidence interval 1.42 to 2.08). Those with a greater frequency of VPCs or complex VPCs had similar rates of HF compared to those with a single VPC and all had rates greater than those with no VPC. In conclusion, in this large population-based cohort, the presence of VPCs was associated with incident HF, independent of incident coronary heart disease.     

Analyse der Mitralringexkursion mittels Gewebedopplerechokardiographie (Tissue Doppler echocardiography = TDE) Nichtinvasive Aufdeckung einer linksventrikul?ren, diastolischen Funktionsst?rung

Summary Background: Mitral inflow velocity, deceleration time, and isovolumic relaxation time recorded by Doppler echocardiography have been widely used to evaluate left ventricular diastolic function but are affected by age, heart rate, loading conditions, and other factors. The diastolic mitral anulus velocity assessed by tissue Doppler echocardiography (TDE) was suggested to provide additional information about LV relaxation less affected by filling pressures. Aim of this study: This study was designed to assess the clinical utility of mitral anulus velocity in the evaluation of left ventricular diastolic function. Patients and methods: Three groups of patients with a systolic ejection fraction > 45 % were separated: 10 normal volunteers (60 - 10 y, CON group), 15 asymptomatic patients with known coronary artery disease (60 - 11 y, CAD group) and 15 patients with longterm arterial hypertension and heart failure symptoms (58 - 9 y, HYP group). The mitral inflow profile (E, A, E/A) was measured by pulsed Doppler, and the deceleration time (DT) and the isovolumic relaxation period (IVRT) were calculated. Systolic, early, and late diastolic velocities of the septal mitral anulus (S_T, E_T, A_T, E_T/A_T) were assessed by pulsed TDE. All study subjects had invasive measurements of left ventricular end diastolic filling pressures during left heart catheterization. Results: In the AH group, E_T (6.9 - 4.8 cm/s) and E_T/A_T (0.71 - 0.28) were reduced compared to the CON group (11.7 - 4.7 cm/s and 1.11 - 0.36, p < 0.05, respectively) and the CAD group (8.9 - 5.4 cm/s and 0.85 - 0.26, respectively, p = ns). The groups did not differ with respect to the mitral E/A ratio, the deceleration time and the isovolumic relaxation time. LVED in the HYP group (16 - 8 mm Hg) was elevated compared to the CON group (8 - 3, p < 0.05) and the CAD group (12 - 6 mm Hg, p = ns). No correlation was found between E_T and LVED (r = 0.26). When the combination of mitral E/A ratio > 1 with LVED S 15 mm Hg was classified as pseudonormalization, the pseudonormalization could be identified by a peak early diastolic mitral anulus velocity (E_T) < 7 cm/s and an E_T/A_T ratio < 1 with a sensitivity of 77 % and a specificity of 88%. Conclusions: The early diastolic mitral anulus velocity assessed by TDE (E_T) is a preload-independent index of LV relaxation. TDE permits the detection of diastolic dysfunction in patients with a pseudonormal mitral inflow and elevated filling pressures. Zusammenfassung Hintergrund: Zur Analyse der linksventrikulären Relaxation werden die früh- und spätdiastolischen Geschwindigkeitsmaxima über der Mitralis (E, A) mit dem gepulsten Doppler abgeleitet sowie die Dauer der Dezelerations- und isovolumetrischen Relaxationszeit bestimmt. Alle genannten Parameter ändern sich jedoch in Abhängigkeit von Alter, Herzfrequenz und Lastbedingungen. Die Erfassung der diastolischen Exkursion des Mitralrings mittels Gewebedopplerechokardiographie (TDE) soll eine lastunabhängige Beurteilung der linksventrikulären, diastolischen Funktion ermöglichen. Ziel der Studie: Ziel der vorliegenden Studie war die Erfassung der diagnostischen Wertigkeit der Mitralringexkusion in der Beurteilung der diastolischen, linksventrikulären Funktion. Patienten und Methoden: Drei Gruppen von Patienten mit einer systolischen Ejektionsfraktion > 45 % wurden untersucht: 10 Kontrollprobanden (60 - 10 J., KON-Gruppe), 15 asymptomatische Patienten mit koronarer Herzerkrankung (60 - 11 J., KHK-Gruppe) und 15 Patienten mit langjähriger, arterieller Hypertonie und Symptomen der Herzinsuffizienz (58 - 9 J., HYP-Gruppe). Das Mitraleinstromprofil (E, A, E/A) wurde mittels gepulstem Doppler gemessen und die Dezelerations- (DT) sowie isovolumetrische Relaxationszeit (IVRT) bestimmt. Systolische, früh- und spätdiastolische Geschwindigkeiten des medialen Mitralanulus (S_T, E_T, A_T, E_T/A_T) wurden mittels gepulstem TDE abgeleitet. Bei allen Patienten wurde im Rahmen einer Linksherzkatheteruntersuchung der linksventrikuläre, enddiastolische Füllungsdruck (LVED) bestimmt. Ergebnisse: In der HYP-Gruppe waren E_T (6,9 - 4,8 cm/s) und E_T/A_T (0,71 - 0,28) im Vergleich zur KON-Gruppe (11,7 - 4,7 cm/s bzw. 1,11 - 0,36, p < 0,05) und zur KHK-Gruppe (8,9 - 5,4 cm/s bzw. 0,85 - 0,26, p = ns) vermindert. Die drei Gruppen unterschieden sich nicht hinsichtlich der mitralen E/A-Ratio, der Dezelerations- und isovolumetrischen Relaxationszeit. LVED war in der HYP-Gruppe (16 - 8 mm Hg) höher als in der KON-Gruppe (8 - 3, p < 0,05) und der KHK-Gruppe (12 - 6 mm Hg, p = ns). Keine Korrelation wurde zwischen E_T und LVED gefunden (r = 0,26). Wenn die Kombination aus mitraler E/A-Ratio > 1 und einem LVEDP S 15 mm Hg als Pseudonormalisierung klassifiziert wurde, identifizierten eine frühdiastolische Mitralringexkursion (E_T) < 7 cm/s und eine E_T/A_T-Ratio < 1 eine Pseudonormalisierung mit einer Sensitivität von 77 % und einer Spezifität von 88%. Schlußfolgerung: Das mit TDE gemessene frühdiastolische Geschwindigkeitsmaximum des medialen Mitralanulus (E_T) ist ein lastunabhängiger Index der linksventrikulären Relaxation. TDE identifiziert die diastolische Funktionsstörung bei Patienten mit pseudonormalem Mitraleinstromprofil und erhöhten Füllungsdrücken.     

Differentiation profile of peripheral blood-derived vascular progenitor cell predicts intimal hyperplasia after coronary stenting

In-stent restenosis is largely due to intimal hyperplasia (IH). The number of vascular progenitor cells (VPCs) mobilized at the acute phase after stenting is associated with IH. This study sought to determine whether the differentiation profile of VPC predicts the development of IH. Peripheral blood was collected in 58 patients after bare-metal stenting to culture VPCs. Intravascular ultrasound was performed to estimate the area of IH 6 months after stenting. VPC differentiation was determined using flow cytometry. VE-cadherin (VE-Cad) and α-smooth muscle actin (α-SMA) were used to identify endothelial and smooth muscle cell lineages, respectively. After culturing, VPCs differentiated into four different phenotypes (α-SMA⁻VE-Cad⁺, α-SMA⁺VE-cad^high, α-SMA⁺VE-cad^low, and α-SMA⁺VE-Cad⁻). IH was correlated with gender (P = 0.04), smoking status (P = 0.04), reference diameter (P = 0.03), minimal lumen diameter (P = 0.03), stent area (P < 0.0001), and parameters in the VPC differentiation profile (P < 0.05). Multivariate analysis controlling for stent area, smoking status, and gender revealed that IH was positively and independently associated with the number of differentiated α-SMA⁺VE-Cad ^low/− VPCs (P < 0.0001), and the ratio of α-SMA⁺VE-Cad ^low/− VPCs to α-SMA⁻VE-Cad⁺ VPCs (P = 0.001). These parameters in the VPC differentiation profile independently predicted the IH and provided additive information to traditional risk factors. In conclusion, the profile of VPC differentiation predicts the severity of post-stent IH and may be a potential tool in the future for clinicians to identify patients at risk of post-stent restenosis.     

The timing of ventricular premature complexes initiating chronic ventricular tachycardia

Prematurity index (PI), defined as the ratio of the coupling to QT intervals of isolated ventricular premature complexes (VPC) and those initiating ventricular tachycardia (VT) on 24-hour ambulatory ECG recording, was examined in 496 episodes of VT occurring in 122 patients. The PI of VPC initiating VT was <1 in only 62 (13%) of the VT episodes and occurred in 14 patients. Although the range of PI was similar for isolated VPC and those initiating VT, for individual patients the PI of VPC initiating VT was significantly longer than the PI of isolated VPC (P<0.01). This relationship was not affected by age, sex, presence of absence of heart disease, or drug therapy.The coupling interval of the first VT complex was longer than the first interectopic interval of the VT (VT₁-VT₂) in 88 (72%) patients; and, the VT₁-VT₂ interval correlated strongly with the average R-R during VT (r=0.75), (p<0.001).The VT was irregular in 48 patients with 300 episodes of VT. Irregularity of the VT was significantly associated with shorter duration of VT (p<0.05).These results show that, for individual patients, the PI of VPC initiating VT tends to be longer than that of isolated VPC, and that the rate of VT is usually predictable from the duration of the first interectopic interval of the VT. These results may have mechanistic implications.     

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.     

Left ventricular end-systolic pressure volume relations in healthy young men

The purpose of the present study was to establish the relationshipof left ventricular end-systolic volume vs. mean systemic pressurein variously afterloaded beats in a group of healthy, young,men (n=6, age 24±0.9 years). The relationship was expressedby the slope (E_max) of the line connecting pressure-volume co-ordinatesand its extrapolated intercept (V_d) of the volume axis. Theslope was calculated by linear regression of mean systemic arterialpressure (mean SAP, measured by catheter in the radial artery)vs. end-systolic left ventricular volume (ESV, estimated fromcross-sectional, 4-chamber echocardiographic images). Recordingswere obtained at resting, reduced (nitroglycerin infusion),and elevated (metaoxedrin infusion) blood pressure. IndividualE_max values ranged from 1.05 to 2.01 mmHg ml^–1; Vd wasconsistently found to be negative, ranging from –4.7 to–54.8 ml. All individual relations were statisticallysignificant (P<005 to P<0001). Group values were E_max=1.27±0.25(SE) mmHg ml^–1, V_d=–43.3±7.5 (SE) ml, andE_max indexed for body surface area, E_{max ind} ±=2.54±0.49(SE) mmHg ml^–1 m^–2. We further examined the validityof proposed optimal relations among E_max, heart rate (HR) andsystemic resistance (R_s): E^max/HR=R_s, and among ejection fraction(EF), EDV and V_d: EF=0.5 (1–EDV/V_d). For the group E_max/HR/0023±0.003and R_s=0016±0004 (mmHg ml^–1 min^–1), i.e.,a deviation from equivalence of 30% (P<0.001). EF (=0.72±0.02)deviated by 18% (P<0001) from its proposed optimum (0.5 (1–V_d/EDV)=0.61=006).     

Prognostic value of left ventricular volume response during dobutamine stress echocardiography

AIMS: An abnormal left ventricular volume response during dobutamineechocardiography identified patients with severe coronary arterydisease. The aim of the study was to assess the prognostic valueof left ventricular volume changes during dobutamine stressechocardiography in 136 patients. MEHTODS AND RESULTS: Endpoints were defined as spontaneous cardiac events at follow-up.Left ventricular end-diastolic and end-systolic volume changes(abnormal response: >10% and >20> decrease, respectively)were compared with other clinical and stress test variables.During 18±7 months of follow-up, 31 cardiac events occurred:12 hard events (cardiac death [n=6 myocardial infarction [n=6])and 19 soft events (unstable angina [n=16] congestive heartfailure [n=3] End-diastolic volume response (P=0·006),diabetes (P=0·008), inducible wall motion abnormalities(P=0·024), end-systolic volume response (P=0·039)and inducible angina (P=0·038) were related to a greaterlikelihood of cardiac events. The Cox regression analysis revealedend-diastolic volume response (odds ratio: 3·0; CI 1·44–6·32)and diabetes (odds ratio: 2·7; CI 1·28–5·69)to be independent predictors of spontaneous cardiac events.Diabetes (odds ratio: 4·0; CI 1·26–12·80)and >40% baseline ejection fraction (odds ratio: 2·21;CI 1·14–4·29) were independent predictorsof hard events. CONCLUSIONS: An abnormal end-diastolic volume response during dobutaminestress echocardiography identifies patients with an unfavourableoutcome; they should be considered for more accurate prognosticstratification.     

Cyclic bursts of ventricular premature contractions of more than one minute intervals.

Ventricular premature contractions (VPCs) occasionally appear successively in the form of bigeminy, trigeminy or quadrigeminy associated with quiescent periods. However, details of these rhythmic VPC bursts have not been well documented. We analyzed the incidence, periodicity and interval of VPC bursts exhibiting bigeminy or trigeminy using ambulatory ECG monitoring and computer analysis. We defined VPC bursts as more than 5 successive groups of VPCs each containing more than 20 VPCs in the form of bigeminy or trigeminy that were interrupted by normal sinus rhythm lasting for more than 60 seconds. Bursts thus defined were observed transiently or continuously in 78 out of 500 consecutive patients showing > 3000 VPCs a day. Their age ranged from 14 to 76 years (mean 48). Forty patients were men and 38 were women. We could discriminate between two types of bursts on the instantaneous heart rate tachograms. Dome type bursts (n = 48) showed gradual shortening of the VPC coupling intervals whereas horizontal type bursts (n = 30) demonstrated fixed coupling intervals during the bursts. Cycle length of the dome type burst was 185 +/- 40 seconds and regular, whereas it was 210 +/- 63 seconds and irregular in the horizontal type (NS). Duration of the VPC bursts was 101 +/- 31 seconds in the dome type and 98 +/- 41 seconds in the horizontal type. Both burst types were associated with transient increases in sinus rate and abbreviated VPC-VPC intervals. We suspect ventricular parasystole to be the mechanism of these bursts especially in the dome type. Recognition of these two burst types from heart rate tachograms may be of value in the suppression of VPCs.     

Influence of haemodynamics and myocardial ischaemia on Doppler transmitral flow in patients undergoing dobutamine echocardiography

To examine whether pulsed Doppler left ventricular filling indicescan reliably detect myocardial ischaemia in patients with coronaryartery disease undergoing dobutamine stress echocardiographywe studied three groups matched for age and global indices ofleft ventricular function. Group 1 patients (n=10) had normalcoronary arteries whereas those in Groups 2 (n=12) and 3 (n=15)had significant coronary disease (70% diameter stenosis) atangiography. After stopping cardiouctive treatment, patientsunderwent incremental dobutamine stress (5, 10, 15 and 20 µg.kg^–1. min^–1) during pulsed Doppler interrogationof diastolic filling with simultaneous heart rate and bloodpressure measurements. Only Group 3 patients developed myocardialischaemia using electrocardiographic and cross sectional echocardiographiccriteria, subset 3A (n=4) comprised those with inducible mitralregurgitation on colour Doppler. Electrocardiographic R-R intervaldecreased (–311 ± 123 ms, P<0·001) andmean blood pressure altered (5±17 mmHg, P=ns) uniformlyacross groups. The respective changes in peak early velocity,peak atrial velocity and their ratio for Groups 1 (0·08± 0·09 m. s^–1, 0·26 ± 0·18m.s^–1 and – 0·32 ± 0·36), 2(0·07 ± 0·07 m.s^–1 0·18±0·15m.s^–1 and –0·13±0·21) and 3(0·09±0·12 m.s^–1, 0·20±0·13m.s^–1 and –0·17±0·21) weresimilar (all P=ns between groups). Corresponding data for subset3A (0·23 ± 0·04 m.s^–1 0·20± 0·10 m.s^–1and 0·00 ± 0·16)revealed a significantly greater increase in peak early velocityand normalized velocity ratio in these patients. Overall, changesin peak early (r= –0·47, P<0·01) andatrial velocity (r–0·65, P<0·001) andtheir ratio (r=0·35, P<0·05) correlated withreduction in R-R interval but not alterations in blood pressure.In conclusion, tachycardia during dobutamine stress masks theeffects of myocardial ischaemia on Doppler diastolic indicesalthough a minority of patients with inducible mitral regurgitationmanifest a relatively distinct filling profile.     

Analysis of intracardiac electrograms showing monomorphic ventricular tachycardia in patients with implantable cardioverter-defibrillators

Ventricular tachycardia (VT) initiation and its relation to various clinical factors was studied by reviewing intracardiac electrograms from patients with implantable cardioverter-defibrillators. Events were divided into (1) sudden onset without preceding ventricular premature complexes (VPCs), (2) extrasystolic onset with VPCs, or (3) paced, depending on the type and morphology of the last 5 beats before initiation of VT. Prematurity index, sinus rate, cycle length, and presence of short-long-short sequence for each episode was noted. A total of 268 episodes of VT among 52 patients were analyzed. Extrasystolic initiation was the most frequent pattern (177; 66%) followed by sudden onset (75; 28%) and paced (16; 6%). Among extrasystolic onset, 99 episodes (56%) were due to multiple VPCs and 149 episodes (84%) had different VPC morphology than the subsequent VT. Among pacing-induced VT, 13 of 16 episodes were due to inappropriate pacing due to undersensing of prior R waves. Sudden-onset episodes were slower (mean cycle length 383+/-97 ms) than extrasystolic (mean cycle length 336+/-88 ms, p = 0.002) and paced (mean cycle length 313+/-85 ms, p = 0.01) onset. Patients in the sudden-onset group had better left ventricular ejection fraction (33+/-15%) than the extrasystolic (29+/-11%, p<0.001) and paced (28+/-14%, p<0.01) groups. Extrasystolic onset with multiple, late coupled VPCs was the most common pattern of VT initiation and was associated with lower ejection fraction. Sudden-onset initiation was more common with better preserved systolic function.