Cardiac anatomy, function and metabolism in elite cyclists assessed by magnetic resonance imaging and spectroscopy

We investigated whether left ventricular hypertrophy in elitecyclists is associated with functional changes or abnormal energymetabolism. Left ventricular hypertrophy is a powerful risk factor for suddencardiac death with different prognostic significance among thevarious geometric forms. Cyclists may have a combination ofmixed eccentric and concentric hypertrophy. Magnetic resonance imaging was used to define left ventricularmass, geometry and function. Thirteen highly trained male cyclistsand 12 healthy controls were investigated. Proton-decoupledphosphorus-31 cardiac spectroscopy was performed to assess parametersof myocardial high-energy phosphate metabolism. Left ventricularmass and end-diastolic volumes normalized for body surface areawere significantly higher in cyclists (124·1 ±9·4 g. m^–2 and 106·2 ± 11·4ml. m^–2, respectively) than in controls (85·9 ±9·3 g. m^–2 and 79·1 ± 11·6ml. m^–2, respectively), (both P<0·0001). Theleft ventricular mass to end-diastolic volume ratio, as a parameterof left ventricular geometry, was not significantly increasedin cyclists compared to controls. Resting left ventricular ejectionfraction, cardiac index, and systolic wall stress in cyclistsdid not differ significantly from those of controls. The phosphocreatineto adenosine triphosphate ratio was not significantly differentbetween cyclists and controls (2·2 ± 0·34vs 2·2 ± 0·17, ns). Cyclists show prominent left ventricular hypertrophy with normalgeometry. The finding that the hypertrophic hearts of the cyclistshad normal left ventricular function and a normal phosphocreatineto adenosine triphosphate ratio suggests that sport-inducedleft ventricular hypertrophy is a physiological adaptation ratherthan a pathophysiological response.     

The haemodynamic side-effects of ionic and non-ionic contrast media in the presence of pulmonary hypertension: experimental and clinical investigation

The haemodynamic side-effects of ionic (amidotrizoate) and non-ionic(iopamidol) constrast media after injection into the right atriumwere compared in experimental and clinical studies.Pulmonaryhypertension was induced in 10 dogs by embolization of the pulmonaryvascular bed with agaragar solution (mean pulmonary artery pressure=44.2mm Hg). Iopamidol (1.5ml kg^-1) caused a moderate decrease inpulmonary and systemic vascular resistance, slight increasesin right ventricular end-diastolic pressure and a marked risein right ventricular contractility (dP/dt_max). Amidotrizoate(1.5ml kg^-1) caused considerable systemic vasodilation and initialincrease in pulmonary vascular resistance and pressure followedby a substantial increase in right ventricular end-diastolicpressure and a decrease in contractility.Central and peripheralhaemodynamics were measured in 20 patients with pulmonary hypertension(mean pulmonary artery pressure=38.1 mm Hg) due to valvularheart disease before and following injections with 40 ml ofboth types of constrast medium in randomized order. Heart rate,cardiac output and right atrial pressure rose significantlymore after amidotrizoate and this constrast medium caused moreextensive systemic vasodilation and a larger decrease in aorticpressure as compared to iopamidol. Pulmonary artery pressurewent up moderately with both contrast media.It is concludedthat non-ionic low-osmolality constrast media like iopamidolinduce less pronounced haemo-dynamic alterations, in particularless increase in right ventricular filling pressure. This maybe beneficial to patients with pulmonary hypertension undergoingangiocardiography or digital subtraction angiography.     

Ventricular tachycardia in myocardial infarction: Relation to heart rate and premature ventricular contractions

Analysis of monitored electrocardiograms, recorded in 77 patientsduring the first 48 hours following the onset of myocardialinfarction, revealed 492 episodes of ventricular tachycardiawith rates of 90–220 min^–1. Characteristics of theventricular tachycardia episodes were correlated with heartrate and with the rate and complexity of ventricular arrhythmiasin the 10-min period preceding ventricular tachycardia. Ventriculartachycardia with rates of 140–180 min^–1 and witha QS configuration was the most frequent event. The first ectopiccomplex of VT was R-on-Tin only 17.2%. Sinus tachycardia wasassociated with significantly fewer episodes of VT with ratesof 110–140min^–1 than when the sinus rate was normal.However episodes of ventricular tachycardia with rates of 181to 220 beats min^–1 were more frequent during sinus tachycardia.Analysis of the frequency of premature ventricular contractionsin the 10-min period immediately preceding ventricular tachycardiarevealed no premature ventricular contractions in 24.4% of cases.Multiple premature ventricular contractions with a frequencyof >5 min^-1 were observed in 8.4% of cases, multifocal in30.3%, couplets in 24% and early PVCs in 12.2%. In the minutebefore ventricular tachycardia, only 40.2% of cases displayedpremature ventricular contractions. In that minute, complexpremature ventricular contractions were distributed as follows:multifocal in 10%, couplets in 8.7% and early PVCs in 2.6% ofcases. Out of the total of 492 runs of ventricular tachycardia,5 cases (1%) resulted in ventricular fibrillation. The frequencyand complexity of premature ventricular contractions as wellas the characteristics of ventricular tachycardia were foundto be of little predictive value for the immediate developmentof ventricular fibrillation in patients with acute myocardialinfarction.     

Arrhythmogenic right ventricular cardiomyopathy: clinical registry and database, evaluation of therapies, pathology registry, DNA banking.

A multidisciplinary collaborative European study has been designedwith the aim to investigate the clinical, pathological and geneticfeatures of arrhythmogenic right ventricular cardiomyopathy(ARVC), which is a progressive, genetically determined disorderof the right ventricular myocardium and a major risk of suddendeath particularly in the young.^1–3 The disease is reportedfamilial up to 50% with autosomal dominant inheritance whilean autosomal recessive form (Naxos disease) associated withcutaneous abnormalities also exists. Nine genetic loci and mutationsin three genes have been discovered so far.^4–7 Treatmentand prevention of ventricular tachyarrhythmias and sudden deathinclude antiarrhythmic drug therapy, catheter ablation and theimplantable cardioverter-defibrillator.^2,8–11 However,a systematic evaluation of treatment options is not yet available.     

Coronary vasodilator reserve in primary and secondary left ventricular hypertrophy: A study with positron emission tomography

Objectives Coronary vasodilator reserve is reduced in hypertrophiccardiomyopathy and secondary left ventricular hypertrophy despiteangiographically normal coronaries. The aim of the present studywas to assess whether quantitative differences exist betweenthese conditions. Methods Using positron emission tomography with H₂¹⁵O, myocardialblood flow was measured at baseline and following intravenousdipyridamole (0·56 mg. kg ^–1) in 12 hypertrophiccardiomyopathy patients (age 34 (11) years, mean (SD), all male),16 secondary left ventricular hypertrophy patients (age 58 (20)years, P<0·01 vs hypertrophic cardiomyopathy; 10 female)and 40 normal controls (age 54 (20), 13 female). In view ofthe known decline of post-dipyridamole myocardial blood flowwith age, myocardial blood flow was compared between the patientgroups and appropriately matched subsets of the total controlgroup. Results Baseline myocardial blood flow in the hypertrophic cardiomyopathypatients was 0·82 (0·23) ml. min^–1 . g^–1vs 0·94 (0·14) ml. min^–1 . g^–1 inits matched control group, P=ns. For the secondary left ventricularhypertrophy patient group, baseline myocardial blood flow was1·17 (0·40) ml . min^–1 . g^–1 vs 1·06(0·28) ml . min^–1 . g^–1 for the secondaryleft ventricular hypertrophy matched control group, P=ns. Followingdipyridamole, myocardial blood flow was 1·64 (0·44)ml . min^–1 . g^–1 in hypertrophic cardiomyopathypatients vs 3·50 (0·95) ml . min^–1 . g^–1forthe hypertrophic cardiomyopathy matched control group, P=0·0001.For the left ventricular hypertrophy patients, post-dipyridamolemyocardial blood flow was 2·27 (0·60)ml . min^–1. g^–1 vs 2·94(1·29) ml . min^–1 . g^–1for the left ventricular hypertrophy controls, P 0·06.Coronary vasodilator reserve (dipyridamole-myocardial bloodflow/baseline-myocardial blood flow) was 2·05 (0·61)for hypertrophic cardiomyopathy patients vs 3·81 (0·98)for the hypertrophic cardiomyopathy controls (P=0 0001, patientsvs controls) and 2·06 (0·62) for left ventricularhypertrophy patients vs 2·90 (1·38) for the leftventricular hypertrophy controls, P<0·03 patientsvs controls. After correction of baseline myocardial blood flowfor baseline heart rate x systolic pressure product, coronaryvasodilator reserve for the hypertrophic cardiomyopathy patientswas 2·06 (1·06) vs 4·34 (1·54) forthe hypertrophic cardiomyopathy controls, P=0·0002 andin the secondary left ventricular hypertrophy patients, thevalues were 2·13 (0·64) vs 2·89 (1·42)in the secondary left ventricular hypertrophy controls, P<0·05. Conclusions In both hypertrophic cardiomyopathy and secondaryleft ventricular hypertrophy, the computed coronary vasodilatorreserve is impaired, even after correction for baseline cardiacwork. However, the extent of the reduction is greater in thehypertrophic cardiomyopathy patients. In the blunting of vasodilatorreserve of secondary left ventricular hypertrophy, the patients'greater hyperaemic response is partly offset by the higher baselinemyocardial blood flow.     

Tissue Doppler and cardiac resynchronisation therapy: a new challenge for the optimal choice of candidates

Dear Editor, With interest, we read the article of Ghio et al.¹ and the Editorialof Breithardt et al.² in which the usefulness of Tissue Doppler(TD) to detect left ventricular (LV) dyssynergy was reported.Ghio et al.¹ defined the intraventricular asynchrony as a differencegreater than     

Left ventricular dyssynchrony and dynamic functional mitral regurgitation: relationship or association?

Numerous parameters are associated with a dismal prognosis inheart failure patients. Some of these factors may be mechanisticallyrelated, such as increased left ventricular (LV) volume, functionalmitral regurgitation (MR), QRS widening, and LV dyssynchrony.Indeed, LV dilation produces distortion of ventricular geometry.The apical and outward displacement of the mitral leaflets restrictstheir ability to close through tethering forces. QRS wideningis frequently associated with LV dyssynchrony. Both dysfunctionand dyssynchrony, notably the dyscoordination of the segmentscontaining papillary muscles¹ reduce LV-generated mitral valveclosing force. Functional MR varies dynamically depending on annular size,loading conditions, and a balance of closing force and mitralvalvular deformation. Dynamic MR can be reliably quantitatedduring exercise testing. Large exercise-induced increases inischaemic MR are associated with acute pulmonary oedema² anda high risk of morbidity and mortality.³ In patients with normalQRS duration     

Improved clinical outcome after intracoronary administration of bone marrow-derived progenitor cells in acute myocardial infarction: final 1-year results of the REPAIR-AMI trial: reply

Recently, Osterziel¹ raised a question about the appropriatenessof the clinical endpoints used in the REPAIR-AMI trial.² Primaryendpoint of the trial was the change in left ventricular ejectionfraction, assessed by LV angiography.³ As such, the REPAIR-AMItrial was designed as a proof-of-concept trial, and intracoronaryinfusion of bone marrow-derived progenitor cells (BMC) is associatedwith improved left ventricular contractile function. Therefore,we are rather puzzled about the disappointment expressed byOsterziel,¹ given that the trial was obviously not powered toand did never claim to detect differences in single clinical     

Leaky ryanodine receptors cause delayed afterdepolarizations and ventricular arrhythmias.

Catecholaminergic polymorphic ventricular tachycardia (CPVT)is an inherited arrhythmogenic disease characterized by theabsence of structural heart disease, syncope, and sudden cardiacdeath.¹ Typically, acceleration of the heart rate during physicalexercise or emotional distress provokes an increasing numberof ventricular premature complexes followed by runs of bidirectionalor polymorphic ventricular tachycardia (VT). During clinicaltesting, about 30–50% of the patients will reproduciblydevelop VT following exercise testing or catecholamine injection.^1,2 The ECG morphology of ventricular tachyarrhythmias observedin patients with CPVT resembles that of VTs commonly describedin digitalis toxicity (which is associated with cellular calciumoverload), and in metabolic disturbances as seen in severe HF(which is associated with high adrenergic tone).³ In conditionsof cytoplasmic Ca²⁺ overload or enhanced ß-adrenergicsignalling, cardiac myocytes exhibit greater ectopic activity.It has therefore been suggested that arrhythmias in CPVT aremediated by triggered activity and delayed afterdepolarizations(DADs),     

Reduction of QRS duration following pulmonary valve replacement in tetralogy of Fallot: implications for arrhythmia reduction?

Tetralogy of Fallot is the commonest form of cyanotic congenitalheart disease, and early outcomes following surgical repairare steadily improving. Nonetheless, these patients remain atrisk for late-onset arrhythmias as well as sudden death.^1,2Increased QRS duration and right ventricular (RV) dilation secondaryto pulmonary regurgitation have both been described as markersfor increased risk of ventricular arrhythmias and sudden death.^3–5Pulmonary valve replacement (PVR) in these patients has been     

Ventricular arrhythmias and athlete's heart: Role of signal-averaged electrocardiography

The aim of this study was to assess the prevalence and the prognosticvalue of ventricular late potentials in apparently healthy top-levelathletes with ventricular arrhythmias, and the effect of physiologicalmyocardial hypertrophy (athlete's heart) on the electrogenesisof the signal-averaged electrocardiogram (ECG). Two groups ofasymptomatic athletes without underlying heart disease werestudied: group A consisted of 35 athletes without arrhythmiasand group B of 25 athletes with frequent and complex ventricular arrhythmias (ventricular ectopic beats >5000. 24 h^–1and ventricular couplets >15 . 24 h^–1). Late potentialswere present if athletes had significantly prolonged filteredQRS and low amplitude signal duration and low root mean squarevoltages at both 25–250 Hz and 40–250 Hz filters.While late potentials were absent in all normal athletes ofgroup A, they were present in seven of 25 (28%) athletes witharrhythmias of group B (P<0·003 Ten of 25 athletes(five with and five without late potentials) of group B underwentprogrammed ventricular stimulation using a protocol comprisingup to three extrastimuli. No episode of sustained ventriculartachycardia was induced. In four of five athletes with latepotentials and in one of five without them, unsustained ventricularresponses were induced. Echocardiographically determined leftventricular mass found in both groups of athletes did not influencethe pathological result of the signal-averaged ECG parameters. This study shows the applicability of the signal-averaged ECGin identifying ventricular late potentials in a selected populationof top-level athletes with frequent and complex ventriculararrhythmias and without overt heart disease; it also shows thatthe presence of late potentials is not influenced by left ventricularmass, even if extreme (>350 g), and it is correlated to anon-sustained ventricular response during an electrophysiologicalstudy.     

Pulmonary valve replacement in patients with tetralogy of Fallot and pulmonary regurgitation: early surgery similar to optimal timing of surgery?

Tetralogy of Fallot is the most common form of cyanotic congenitalheart disease, with a prevalence of 0.26–0.8 per 1000live births.¹ Total repair for tetralogy of Fallot has beenavailable for 50 years with a favourable outcome in most patients.Today, one is faced with an increasing number of patients withresidual pulmonary regurgitation. It was previously thoughtthat pulmonary regurgitation in Fallot patients was rather harmless.However, accurate measurements of right ventricular volumesusing cardiovascular magnetic resonance (CMR) imaging have visualizedimportant enlargement of the right ventricle in patients withsevere pulmonary regurgitation.² Moreover, it has been recentlydemonstrated that pulmonary regurgitation leads to progressiveright ventricular dilatation and, with time, to right ventricular     

Efficacy of flecainide in pacing-induced sustained ventricular tachyarrhythmias: correlation to clinical parameters and tachycardia-characteristics

Seventy-two patients with sustained ventricular tachycardiaor syncope of unknown origin underwent electrophysiologic evaluationbefore and after therapy with flecainide (200–300 mg day^–1).In all patients, sustained ventricular tachycardia or ventricularfibrillation was inducible during control electrophysiologicstudy. During flecainide therapy, sustained ventricular tachycardia(VT) was no longer inducible in 18 patients (25%) whereas in54 patients, VT was still inducible. In five of the latter patients,VT became more difficult to induce (overall efficacy 32%). Therate of VT decreased from 214±49 beats min^–1 duringthe control electrophysiologic study to 178±48 beatsmin^–1 during flecainide (P<0.01). The ERP of the rightventricle increased from 251±27 ms during the controlstudy to 267±34 ms on flecainide (P<0.01). Mean ejectionfraction and mean LVEDP did not differ between responders andnon-responders, yet the presence of a left ventricular aneurysmcorrelated with a lack of antiarrhythmic response to flecainide.VT rate as well as VT morphology during the control study discriminatedbetween responders and non-responders; 11% of patients withVT-rate 230 beats min^–1 responded to oral flecainidecompared with 31% with a VT rate > 230 beats min^–1at control. 26% with induced monomorphic VT responded, comparedwith 100% with induced VF during the control study. 18 of 23responders were discharged on flecainide. During a mean follow-upof 26±18 months, two patients experienced a recurrenceof VT and in one patient, flecainide had to be discontinueddue to side-effects. Thus, the acute efficacy of flecainide, evaluated by serialdrug testing, correlates with haemodynamic parameters and thecharacteristics of tachycardia.     

Effect of isoproterenol on serum potassium and magnesium

Some ventricular arrhythmias can be related to a decrease inthe level of potassium (K) and/or magnesium (Mg). Because adrenergicstimulation decreases serum K⁺ and Mg⁺⁺, we decided to investigatethe effects of a beta-receptor agonist, isoproterenol, on serumK⁺ and Mg⁺⁺, and their consequences on the induction of tachycardia.Programmed atrial and ventricular stimulation was performedin 95 patients before and during infusion of 1.6µg . ml^–1of isoproterenol. During isoproterenol infusion, 61 patientshad no inducible tachycardias (group I) and 34 had induciblesustained tachycardias (group II): 16 of them (group IIA) hadinducible sustained supraventricular tachyarrhythmias and 18(group IIB) had inducible sustained ventricular tachycardia.Serum K⁺ and Mg⁺⁺ were measured at the end of stimulation inthe control state and during isoproterenol infusion. The basalvalues in groups I and II did not differ (3.8 + 0.38 vs 3.86+ 0.39 mEq . 1^–1 for K⁺, and 20.18 + 2.68 vs 19.83+1.63mg l^–1 for Mg⁺⁺). Isoproterenol infusion induced a significant(P<0.001) hypokalaemia in all groups and a decrease in serumMg in group II: there was a significant decrease in serum Mg⁺⁺(P<0.05) in group IIA (19.55±1.7 vs 20.4 + 4.6). Thedecrease in serum Mg⁺⁺ in group IIB (18.9+1.55 vs 19.32 + 1.63)was not significant. However the serum Mg⁺⁺ level during isoproterenolinfusion was significantly lower in group IIB than in groupI. In conclusion, the infusion of isoproterenol was responsiblefor a significant hypokalaemia, which did not explain the inductionof tachycardia. On the other hand, it also induced a decreasein serum Mg⁺⁺, which might facilitate the induction of supraventricularand ventricular tachycardia.     

Assessment of ventricular dyssynchrony: global or regional function?

A common cliché states that if you stand still every10 years, you will find yourself in the forefront of fashion.Thus it seems with the analysis of ventricular function. Ithas been recognized for many years that incoordinate or non-uniformcontraction reduces global left ventricular (LV) function. Wiggersdemonstrated in 1922 that stimulation from a ventricular focusrather than supraventricular produced a reduced pulse pressure,prolonged isometric contraction, and systolic ejection timein normal hearts. Although regional wall motion abnormalitieswere recognized early in ischaemic heart disease, it was alsodemonstrated later that it occurs in dilated or hypertrophiccardiomyopathy.¹ However, the realization that asynchronouswall motion due to delayed activation such as in the presenceof a left bundle branch block profoundly affected global functiondid not take place until more recently.² Developments in cardiacimaging     

Myocardial infarct size: correlation with cardiac arrhythmias and sudden death

The study was made in order to determine the relationship betweenmyocardial infarct size and the incidence of cardiac arrhythmiasduring acute myocardial infarction (AMI). In 317 consecutivelyadmitted patients infarct size was estimated from serial serumCK-MB measurements. The ECG was continuously monitored during18 days in hospital, and all electrocardiographic recordingswere analysed daily. All patients were followed up one yearafter discharge. The median infarct size was larger among the 220 patients witharrhythmias than among the 97 patients without (814 Ul^–1vs 419 Ul^–1, P<0.0001). There was a significant relationshipbetween the estimated infarct size and the following arrhythmias:ventricular ectopic beats, sinus tachycardia, and atrioventricularblock, whereas supraventricular ectopic beats showed no suchrelation. Patients with heart failure, however, had a high incidenceof ventricular arrhythmias regardless of the size of their infarcts.The follow-up study demonstrated that the ventricular arrhythmiaspositively correlated with infarct size were also associatedwith significantly increased one-year mortality among hospitalsurvivors. Thus, the present study indicates that not only pump failure,but also cardiac arrhythmias are connected with the negativeinfluence of infarct size on prognosis.     

Prenalterol in primary dilated cardiomyopathy: hemodynamic and angiographic evaluation

The hemodynamic effects of an acute infusion of prenalterol(PN), a new inotropic beta-adrenoceptor agonist, have been evaluatedby cardiac catheterization in 10 patients with primary dilated(congestive) cardiomyopathy. A single dose of20µg/kg wasadministered over 5 min after basal hemodynamic and angiographicmeasurements. The administration of prenalterol caused a significantincrease in mean cardiac index, from 2.3 to 3.3 l/min/m² (P< 0.01) and mean stroke volume, from 47 to 62 ml (P <0.01) without a change in heart rate. Mean left ventricularend-diastolic pressure was reduced from 19 to 13 mm Hg (P <0.05) and left ventricular dp/dt rose from 902 to 1089 mm Hg/s(P < 0.01). Stroke work index increased from 27 to 40 gm/m²(P < 0.01) and ejection fraction from 31 to 36% (P < 0.05).Mean blood pressure did not change and the systemic vascularresistance decreased from 24 to 17 RU (P < 0.01). The favorableeffect of prenalterol on left ventricular relaxation was shownby an increase of peak negative left ventricular dp/dt from946 to 1159 mm Hg/s and by a decrease of the time constant ofleft ventricular pressure fall from 49 to 39 s. These results demonstrated a positive inotropic effect of prenalterolon patients with diffuse and severely reduced contractility.     

Abnormal myocardial deformation properties in obese, non-hypertensive children: an ambulatory blood pressure monitoring, standard echocardiographic, and strain rate imaging study: reply

We thank Song very much for the interest in our work.¹ In ourstudy, we demonstrated a significant increase in left ventricular(LV) circumferential end-systolic     

Safety of dobutamine stress echocardiography: A 24 h Holter monitoring study

BACKGROUND: Dobutamine-atropine stress echocardiography is an efficientmethod in the evaluation of patients with coronary artery disease.However, because high-dose dobutamine is potentially arrhythmogenic,the safety of this stress modality has been questioned. METHODS: We performed a 24 h Holter monitoring, before and immediatelyafter this test, in 73 consecutive patients (60 men and 13 women),mean age 60 ± 12 years. Twentyeight patients had hada recent myocardial infarction, 25 had stable chronic angina,10 chronic ischaemic cardiomyopathy and 10 idiopathic dilatedcardiomyopathy. Dobutamine was progressively increased (5–40µg . kg^–1. min^–1) and atropine was injectedin 30 patients. Arrhythmias and ST-segment deviation beforeand after the stress test were evaluated. RESULTS: The mean peak dobutamine dose was 32 ± 11 µg .kg^–1. min^–1. The heart rate at rest and at peakdose was, respectively, 69 ± 16 and 110 ± 28 beats.min^–1. Side effects during the injection of dobutaminewere mainly ventricular (n=14) or atrial (n=4) premature contractions.Three patients had non-sustained ventricular tachycardia andfive had hypotension during the test. No sustained episode ofsupraventricular or ventricular tachycardia was observed duringthe study. Nonsustained supraventricular and ventricular tachycardiaswere detected in 8 and 21 patients before and in 11 and 16 patientsafter dobutamine stress echocardiography (P=ns). AsymptomaticST-segment deviation was observed in two patients before andfour after dobutamine stress echocardiography. An increase intotal ischaemic time (20 vs 102 mn) was observed after the test,but only five patients had ST modifications. A separate analysisof patients with and without beta-blocker did not alter theseresults. In addition, when the occurrence of significant arrhythmiaswas stratified according to a left ventricular ejection fractionthreshold of 45%, we observed no difference in frequency andseverity of cardiac arrhythmias. CONCLUSION: This study demonstrates that dobutamine stress echocardiographydoes not significantly increase arrhythmia during the following24 h. Further studies are required to evaluate the influenceof the test on ST-segment modification during the same period.