A prospective, randomized comparison of temperature-controlled vs manually delivered radiofrequency catheter ablation in patients undergoing atrioventricular nodal modification or accessory pathway ablation

AIMS: In a prospective, randomized study, the effect of temperaturecontrol on radiofrequency catheter ablation was compared in69 patients undergoing atrioventricular nodal modification (n=32)or ablation of an accessory pathway (n=37) METHODS AND RESULTS: Thirty-five patients were randomized to temperature control,34 to manually delivered radiofrequency ablation. The successrate was 92·5% for accessory pathway ablation and 100%for atrioventricular nodal modification. Mapping duration wassignificantly reduced only in patients undergoing atrioventricularnodal modification. The number of applications was higher formanually delivered ablation in patients undergoing atrioventricularnodal modification (5·6 ± 1·1 vs 1·9± 0·4, P=0·004) as was the cumulative energydelivered (5034 ± 1008 vs 2054 ± 517 W, P=0·013)whereas the mean power per application was higher with temperaturecontrol (41·4 ± 1·8 vs 34·1 ±1·1 W, P=0·002). No significant differences inthese parameters were found in patients undergoing accessorypathway ablation. Coagulum formation on the catheter tip wasobserved more often with manually delivered ablation 5·3%vs 0·9%, P=0·026). The success rate with the initiallyrandomized application mode was higher for temperature control(94·3 vs 61·8%, P=0·003). CONCLUSION: Temperature control during radiofrequency current ablation significantlyreduces mapping duration, necessary applications and cumulativeenergy in atrioventricular nodal modification, but not accessorypathway ablation. Coagulum formation on the catheter tip stilloccurs but is significantly reduced compared to manually deliveredradiofrequency current.     

Dyspnoea and exercise intolerance during cardiopulmonary exercise testing in patients with univentricular heart: The effects of chronic hypoxaemia and Fontan procedure

BACKGROUND: Patients with univentricular hearts have decreased exercisetolerance and may demonstrate exertional dyspnoea. It is notknown if chronic hypoxaemia exacerbates exercise intoleranceand contributes to symptomatic limitation. The extent to whichsurgical correction of a right-to-left shunt by a Fontan-typeprocedure can increase exercise tolerance by reducing arterialdeoxygenation is not well documented. The cardiopulmonary exerciseresponses and the symptomatic status in two groups of univentricularpatients, those who are cyanotic and those who are acyanoticwith Fontan-type circulation, were compared. METHODS AND FINDINGS: Cardiopulmonary exercise testing was performed in 10 univentricularpatients with rest or stress-induced cyanosis (age 30·5±2·3[SE] years; 5 men) who had palliative or no surgery and eightpatients (age 29·4±1·5 years; 4 men) withFontan-type circulation. Peak oxygen consumption was comparablein both groups of univentricular patients (21·7±2·5vs 21·0±1·9 ml. kg^–1 . min^–1,P=0·85) but was less than an age-matched group of 10healthy subjects (34·7±1·9 ml. kg^–1. min^–1, P<0·001 for both). Arterial oxygensaturation was 90·6% at rest in the cyanotic patientscompared with 95·1% in the Fontan patients (P<0·001)and at peak exercise, 66·2% compared with 90·5%(P<0·001). Using a modified Borg scale (0–10),the symptoms of dyspnoea and fatigue were also assessed duringexercise in the patient groups. The Borg scores for dyspnoeain the cyanotic and the corrected univentricular patients were,respectively, as follows: Stage 1: 0·5 vs 1·7;P=0·04; Stage 2: 1·8 vs 2·3, P=0·5;Stage 3: 3·0 vs 3·5, P=0·7; Peak Exercise:4·9 vs 4·8, P=0·9. In addition, the Borgscores for fatigue were: Stage 1: 0·4 vs 1·6,P=0·08; Stage 2: 2·0 vs 2·2, P=0·9;Stage 3: 3·0 vs 4·3, P=0·5; Peak Exercise:4·9 vs 5·4, P=0·5. The major limiting symptomat peak exercise was dyspnoea in four cyanotic patients comparedwith one in the Fontan group (Chi-square 0·982, P>0·10).The arterial oxygen desaturation at peak exercise in the cyanoticpatients limited by dyspnoea was not different from those limitedby fatigue (67·5±10·1% vs 66·7±13·7%,P=0·92). Exercise tolerance was also not related to thearterial oxygen saturation at peak exercise (r=0·47,P=0·17) in these patients. CONCLUSION: Despite correction with Fontan-type surgery, the exercise toleranceand symptoms of these univentricular patients remained similarto those who were cyanosed. Cyanotic patients have adjustedto chronic hypoxaemia and it does not appear to determine theexercise tolerance or the genesis of dyspnoea in these patients.Further randomized prospective studies are required to investigatethe long-term benefits of Fontan-type procedures in these patientson exercise tolerance, symptoms and prognosis.     

Balloon mitral valvotomy: comparison between antegrade Inoue and retrograde non-transseptal techniques

AIMS: The results of percutaneous mitral valvotomy performed by theantegrade transseptal method using the Inoue balloon (n=1000;group 1) and by the retrograde non-transseptal technique usinga polyethylene balloon (n=100; group 2) were compared in a retrospective,non-randomized study. METHODS AND RESULTS: Both the groups were similar with respect to baseline characteristics.The success rate was 95% in group 1 and 93% in group 2. Therewas a significant increase in mitral valve area estimated byGorlin's equation (Group 1: from 0·8 ± 0·5to 2·1 ± 0·8 cm²; Group 2: from 0·8± 0·3 to 1·9 ± 0·8 cm², bothP<0·001) and by Doppler echocardiography using thepressure half-time method (Group 1: from 0·9 ±0·4 to 2·2 ± 0·6 cm²; Group 2: from0·9 ± 0·3 to 2·0 ± 0·7cm², both P<0·001). However, the calculated immediatepost-valvotomy mitral valve area was larger with the Inoue technique(2·1 ± 0·8 vs 1·9 ± 0·8cm²; P<0·02). Results were considered optimal whenthe mitral valve area increased to 1·5 cm², the percentageincrease was 50, and mitral regurgitation was 2/4. Out of thetotal successful procedures, optimal results were obtained in95% patients in Group 1 and 94% in Group 2. Incidence of significantmitral regurgitation (grade 3/4) was similar in two groups (Group1: 4% vs Group 2: 5%, P=ns). A significant left to right atrialshunt (Qp/Qs 1·5:1) in 2·5% and tamponade in2% of cases occurred exclusively with the Inoue technique, whileconduction disturbances, such as transient (<24 h) left bundlebranch block (28%) and complete heart block (2%) were notedwith the retrograde technique (Group 2). Local complicationswere significantly higher in Group 2 (3% vs 0·5%, P<0·01).The procedure time with the Inoue technique was shorter thanwith the retrograde (Group 1: 15 ± 8, range 10 to 35min; Group 2: 22 ± 14, range 15 to 45 min, P=0·05).Echocardiographic follow-up at 1 year showed no significantdifference in mitral valve area between the two groups (Group1 (n=300): 1·8 ± 0·8 vs Group 2 (n=60):1·9 ± 0·9 cm²; P=0·3). CONCLUSION: Balloon mitral valvotomy using the Inoue balloon and the retrogradenon-transseptal technique results in significant immediate haemodynamicand symptomatic improvement. The Inoue technique achieved alarger immediate post-valvotomy mitral valve area, but the differencewas not apparent at 1 year follow-up. Incidence of significantmitral regurgitation was similar with both the techniques; however,local complications occurred more frequently with the retrogradetechnique. Both techniques may complement each other in technicallydifficult cases.     

A randomized trial of a fixed high dose vs a weight-adjusted low dose of intravenous heparin during coronary angioplasty

AIMS: Prospectively to compare success rate and complications in percutaneoustransluminal coronary angioplasty using two doses of heparin. METHODS AND RESULTS: Four hundred patients undergoing coronary angioplasty were randomlyassigned to receive 15 000 IU (group A) or 100 IU. kg ^–1(group B) of heparin. The angioplasty success rate was 95% inboth groups. Stents were placed in 28·5% and 26·5%of patients in groups A and B, respectively (P=0·73).The primary endpoint (freedom from death, myocardial infarction,unplanned revascularization or bailout stenting) occurred in91% vs 95% of patients in groups A and B, respectively (oddsratio: 1·88, 95% CI: 0·80—4·50, P=0·12).Haemoglobin loss was 0·36 ± 1 and 0·27± 0·9 g. dl ^–1 in groups A and B, respectively(P=0·37). The time to sheath removal (735 ± 265vs 558 ± 246 min) and the time to transfer to a stepdownunit (12·7 ± 4·5 vs 9·8 ±4·2 h) were longer in groups A (P=0·0001 for bothcomparisons). CONCLUSION: A weight-adjusted low dose of intravenous heparin is at leastas safe as a fixed high dose for coronary angioplasty. It allowsearlier sheath removal and discharge to a stepdown unit.     

Severe mitral regurgitation complicating acute myocardial infarction: Clinical and angiographic differences between patients with and without papillary muscle rupture

AIMS: To assess the differential clinical and angiographic characteristicsof patients with severe mitral regurgitation related (n=31)or unrelated (n=16) to papillary muscle rupture complicatingacute myocardial infarction. MEHTODS AND RESULTS: The clinical and angiographic features of patients with myocardialinfarction and severe mitral regurgitation were evaluated. Patientswith papillary muscle rupture were older (67 vs 60 years, P>0·005)and had a lower rate of diabetes (7% vs 38%, P>0·005)and of previous angina or infarction (24% vs 50%, P>0·05).Frequency of inferior infarction was high and comparable inboth groups (papillary muscle rupture, 72% vs non-papillarymuscle rupture, 88%, ns) whereas in-hospital rate of angina/infarctextension prior to mitral regurgitation, also high, tended tobe higher in patients without than in those with papillary musclerupture (67% vs 39%, ns). Incidence of multivessel disease tendedto be higher in patients without papillary muscle rupture (87%vs 56%, P>0·06) and they had a lower ejection fraction(46 ± 15 vs 61 ± 14%, P>0·03), whereasthe culprit artery was mainly the right or the circumflex coronaryartery in both groups (papillary muscle rupture, 100% vs nonpapillary muscle rupture, 93%, ns). Valve replacement was performedearlier in patients with papillary muscle rupture (1(1; 14)vs 25 (5; 45) days, median, P>0·002) but was associatedwith a similar mortality (papillary muscle rupture 11/24, 46%vs non-papillary muscle rupture, 7/15, 47%, ns). The main causeof death was cardiogenic shock in patients without papillarymuscle rupture (5/7, 71%), and respiratory insufficiency-sepsisin those with papillary muscle rupture (7/11, 64%). CONCLUSIONS: Severe mitral regurgitation in myocardial infarction with orwithout papillary muscle rupture is mostly related to inferiorinfarction and often follows reinfarction, particularly in non-papillarymuscle rupture cases. The main contributors to surgical mortalityappear to be respiratory insufficiency in patients with papillarymuscle rupture and cardiogenic shock, facilitated by a lowerejection fraction, a higher frequency of diabetes and more extensivecoronary disease, in patients without papillary muscle rupture.     

Physical training improves exercise capacity in patients with mitral stenosis after balloon valvuloplasty

BACKGROUND: Haemodynamic measurements taken at rest and during exerciseshowed that percutaneous transvenous mitral commissurotomy resultsin both acute and long-term improvement. However, the time lagbefore there is an increase in exercise and in peak oxygen uptakeappears to be delayed and irregular. PATIENTS AND METHODS: To assess the potential of physical training to restore betterphysical capacity after percutaneous transvenous mitral commissurotomy,26 patients with mitral stenosis were studied after the procedure.The group was split into two. Thirteen underwent a 3-month rehabilitationprogramme, and the other 13, who did not, acted as controls. RESULTS: The mitral valve orifice area increased similarly, from 1·;12±017to 1·88 ±0·28 cm² in the training groupand from 1·04±0·16 to 1·88±0·19cm² in the control group. Cardiopulmonary parameters were similarbefore percutaneous transvenous mitral commissurotomy (peako₂: 19·9±2·4 vs 18·9±4·5ml. min^–1. kg^–1; peak workload: 94·6±29·3vs 96·1±25 watts; o₂ at anaerobic threshold: 17±3·4vs 16·1±5·2 ml. .min^–1. kg^–1;all P=ns). Three months later the results were higher in thetraining group (peak o₂: 26·6±4·7 vs 21·6±3·8ml. min^–1. kg^–1, P=0·001; peak workload:125·4±26·6 vs 108·5±23 watts,p=0·03; o₂ at anaerobic threshold: 19·6±5·8vs 15·8±2·9 ml. min^–1. kg^–1;P=0·02). CONCLUSION: These results indicate that patients should take up exerciseafter successful percutaneous transvenous mitral commissurotomyfor better functional improvement.     

Heart rate variability as a means of assessing prognosis after acute myocardial infarction: A 3-year follow-up study

AIMS: The present study evaluated the prognostic value of heart ratevariability after acute myocardial infarction in comparisonwith other known risk factors. The cut-off points that maximizedthe hazards ratio were also explored. PATIENTS AND METHODS: Heart rate variability was assessed with 24 h ambulatory electrocardiographyin 74 patients with acute myocardial infarction, 4±2days after hospital admission and in 24 healthy controls. Patientswere followed for 36±15 months. RESULTS: During follow-up, 18 patients died, nine suffered a non-fatalinfarction and 20 underwent revascularization procedures. Heartrate variability was higher in survivors than in non-survivors(P=0·0005) This difference was found at higher statisticallevels when comparing non-survivors vs controls (P=0·0002)A similar statistically significant difference was also foundbetween survivors vs controls (P=0·04). Patients sufferingnon-fatal infarction and cardiac events (defined as death, non-fatalinfarction or revascularization) had a lower heart rate variabilitythan those without (P=0·03 and P=0·03, respectively).With multivariate regression analysis, decreased heart ratevari ability independently predicted mortality and death ornon-fatal infarction. The presence of a left ventricular ejectionfraction <40% and a history of systemic hypertension were,however, stronger predictors. The cut-off points that maximizedthe hazards ratio using the Cox model differed from those reportedby others. CONCLUSIONS: Decreased heart rate variability independently predicted poorprognosis after myocardial infarction. However, the cut-offpoints that should be used in clinical practice are still amatter for further investigation.     

Pro-inflammatory cytokines and endothelium-dependent vasodilation in the forearm. Serial assessment in patients with congestive heart failure

Background In patients with heart failure endothelium-dependent vasodilationof the forearm conduit vessels is impaired possibly becauseof elevated plasma levels of pro-inflammatory cytokines. Theeffect of elevated plasma cytokines on endothelium-dependentvasodilation of forearm conduit vessels was therefore seriallyinvestigated in 16 patients with congestive heart failure duringan episode of acute failure and at the time of recompensation. Methods and Results Pro-inflammatory cytokine levels and hyperaemic brachial arterydiameters were obtained shortly after admission for an episodeof acute heart failure and 11±3 days later at the timeof recompensation, which was obtained using diuretic therapywithout changing other cardiovascular medications. Serum concentrations(Mean±SD) of tumour necrosis factor alpha (TNF-) (decompensationvs recompensation: 25±23pg.ml^–1vs 26±17pg.ml^–1)and interleukine 6 (IL-6) (decom-pensation vs recompensation:27±24pg.ml^–1vs 20±18pg.ml^–1), determinedin venous blood using immunoradiometric assays were elevatedbut remained unaltered following recompensation. Brachial arterydiameter, derived from high-resolution ultrasound scans at restand during reactive hyperaemia, 90s after forearm cuff deflation,increased significantly during reactive hyperaemia at the timeof admission (3·4±0·7mm vs 4·0±0·5mm;P=0·014)and following recompensation (3·4±0·5mmvs 3·8±0·2mm;P=0·032). The brachialartery diameter during recompensation expressed as a percentageof the baseline value was similar at both intervals (decompensationvs recompensation: 117±14% vs 116±10%;P=ns). Atthe time of decompensation, the correlation between TNF- andthe percentage change in brachial artery diameter followingreactive hyperaemia was absent (r=0·098;P=0·719).The same correlation became significant at the time of recompensation(r=0·750;P=0·001). Conclusions In patients with congestive heart failure, plasma levels ofpro-inflammatory cytokines correlate with endothelium-dependentvasodilation of the brachial artery following recompensation,but not during an acute episode of heart failure.     

Assessment of accuracy of the Doppler pressure half-time method in the estimation of the mitral valve area immediately after balloon mitral valvuloplasty

AIM: The reliability of Doppler echocardiography in determining themitral valve area after balloon mitral valvuloplasty has beenquestioned, as discrepancies were noted between measurementsobtained by the pressure half-time method and those derivedhaemodynamically, immediately following completion of the procedure.Recent investigations, however, have indicated that these discrepanciesmay be attributable to the over-estimation of the mitral valvearea by haemodynamic measurements, caused by the presence ofthe iatrogenic atrial septal defect complicating transseptalcatheterization. The aim of the present study was to furthertest this hypothesis. METHODS AND RESULTS: Measurements of the mitral valve area by the Doppler pressurehalf-time method and the Gorlin formula were obtained and comparedin 238 consecutive patients before and immediately after retrogradenon-transseptal balloon mitral valvuloplasty, which does notinvolve puncture and/or dilatation of the inter-atrial septum.No significant difference was found between Doppler- and Gorlin-derivedmeasurements, neither before (1·04±0·23vs 1·03±0·23cm², P=ns) nor immediatelyafter (2·14±0·47 vs 2·12±0·49cm², P=ns) valvuloplasty. Linear regression analysis demonstrateda high degree of correlation between Doppler and Gorlin measurementsbefore (r=0·778) and after (r=0·886) the procedure.Good agreement was confirmed by the Bland—Altman method. CONCLUSION: Doppler echocardiography yields accurate measurements of themitral valve area immediately after retrograde non-transseptalballoon mitral valvuloplasty. This finding supports the hypothesisthat the creation of an iatrogenic atrial septal defect duringtransseptal catheterization may contribute to the poor agreementbetween Doppler and Gorlin data after balloon mitral valvuloplasty.     

Hyperleptinaemia in chronic heart failure: Relationships with insulin

Background Leptin, a product of theobgene, is known to increaseenergy expenditure. Given that chronic heart failure is a hypercatabolicstate, we sought to determine whether congestive heart failureinvolves elevations in plasma leptin levels. Since leptin secretionis up-regulated by insulin, we also explored whether in congestiveheart failure, a hyperinsulinaemic state, plasma leptin levelsrelate to plasma insulin levels. Methods Male patients with weight-stable congestive heart failure(n=25, aged 55·5±2·0, mean±SEM,body mass index=27·4±0·8, radionuclideleft ventricular ejection fraction=29·3±3·0%)and 18 controls, matched for age, sex and body fat (dual energyX-ray absorp-tiometry), underwent measurement of fasting plasmaleptin (radioimmunoassay) and insulin levels. Results Compared to controls, patients with congestive heartfailure had higher plasma leptin [8·12 (–1·12,+1·31)vs 4·48 (–0·61,+0·70) ng.ml^–1,mean±asymmetrical SEM,P=0·003], 41·5% higherplasma leptin per percent body fat mass (P<0·001),and higher fasting insulin levels [67·8 (–11·1,+13·3)vs 32·9 (–5·7,+6·9) pmol.l^–1,P=0·010].In the congestive heart failure group, plasma leptin correlatedwith total body fat (r=0·66) and fasting insulin (r=0·68)(bothP<0·001). In multivariate regression analysesof the congestive heart failure group, fasting insulin (standardizedcoefficient=0·41,P=0·011) emerged as a predictorof plasma leptin levels, independent of total body fat (standardizedcoefficient=0·73,P=0·002, R²=0·66,P<0·001). Conclusions Plasma leptin levels are raised in patients withcongestive heart failure. The observation of a positive relationshipbetween plasma leptin and insulin concentrations suggests thatthe insulin–leptin axis may be related to the increasedenergy expenditure observed in patients with congestive heartfailure.     

Skeletal muscle function at low work level as a model for daily activities in patients with chronic heart failure

AIM: Metabolic exercise abnormalities have been reported in chronicheart failure patients. This study sought to evaluate whetherthese abnormalities affected daily activity. METHODS AND RESULTS: In 16 patients with moderate-to-severe chronic heart failureand in eight controls we measured femoral flow (thermodilution)and metabolism (glucose, lactate, free fatty acids, blood gasvalues) at rest and during a constant load of 20 W, which maymimic a daily activity. At rest, chronic heart failure patientshad a leg flow similar to controls, but showed a higher legoxygen consumption (4·6±0· vs 2·6±0·4ml. min^–1; P>0·05), a higher arteriovenous oxygendifference (7·2±0·5 vs 5·4±0·7ml . d1^–1; P>0·05), and a lower femoral veinpH (7·37±5·–03 vs 7·42±0·01;P=0·01). At 20 W, chronic heart failure patients hada leg flow similar to controls, but showed increased lactaterelease (from resting 11·7±33 to 142+125 µg. min^–1 P>0·0001 vs controls, from resting 5·7±15·4to 50±149 µg . min^–1 ns), higher arterialconcentration of free fatty acids (781±69 vs 481±85µmol . 1^–1; P>0·01), lower femoral veinHCO₃ (24·1+2·6 vs 26·3±1·7mmol .1^–1;P>0·05) and base excess (–2·3+2·3vs –0·24±1·7 mmol . 1^–1 P=0·01 CONCLUSION: In chronic heart failure patients, the important cellular metabolicalterations already present at rest partially affect daily activities,owing to a further decrease in the efficiency of muscle metabolicprocesses, and may preclude tolerance of heavier activities.Such alterations appear, at least in part, independent of peripheralhaemodynamic responses to exercise.     

Effects of antianginal therapy with a calcium antagonist and nitrates on dobutamine--atropine stress echocardiography: Comparison with exercise electrocardiography

BACKGROUND: Anti-ischaemic therapy with nitrates and/or calcium channelblockers profoundly affects the results of pharmacological stressechocardiography with coronary vasodilators but the influenceon catecholamine stress testing remains unsettled. AIMS: The present study aimed to assess the effects of non-beta-blockerantianginal therapy on dobutamine (up to 40 µg.kg^–1.min^–1)-atropine(up to 1 mg) stress echocardiography and to evaluate whetherdrug-induced changes in the dobutamine-atropine stress echocardiographyresponse may predict variations in exercise tolerance. METHODS: Twenty six patients with angiographically assessed coronaryartery disease (seven patients with single-, 10 with double-,and nine with triple-vessel disease) performed a dobutamine-atropinestress echocardiography and an exercise electrocardiographytest in random order both off and on antianginal drugs (nitratesand calcium antagonists). In dobutamine-atropine stress echocardiography,we evaluated: dobutamine time (i.e. the time from initiationof the dobutamine infusion to obvious dyssynergy), wall motionscore index (in a 16-segment model of the left ventricle, eachsegment ranging from 1=normal, to 4=dyskinetic), and rate-pressureproduct at peak stress. RESULTS: Dobutamine-atropine stress echocardiography positivity occurredin 26 out of 26 patients off and in 23 patients on therapy (100vs 88%, P=ns). Atropine coadministration was needed to evokeecho positivity in no patient off and in five out of 26 on therapy(0 vs 19%, P<0·01). The achieved rate-pressure productduring dobutamine-atropine stress echocardiography was comparableon and off therapy (17±4 vs 19±5x10³ mmHgxheartrate. min^–1, Pns). Therapy induced an increase in dobutaminetime (on=16±3 vs off=13±3 min, P<0·01)and a decrease in peak wall motion score index (on=1·3±0·2vs off=1·5±0·3, P<0·01). Thetherapy-induced changes in exercise time during the exerciseelectrocardiography test were not significantly correlated todobutamine-atropine stress echocardiography variations in eitherdobutamine time (r=0·07, P=ns), or peak rate-pressureproduct (r=0·24, P=ns), or peak wall motion score index(r=0·02, P=ns). CONCLUSION: (1) non-beta-blocker antianginal therapy only modestly reducesdobutamine-atropine stress echocardiography sensitivity, althoughatropine coadministration is more often required to reach stressecho positivity under therapy; (2) therapy reduces the severityof dobutamine-atropine stress echocardiography ischaemia stratifiedin the time and space domain, but these changes are only poorlycorrelated to variations in exercise tolerance.     

Functional role of microvascular integrity in patients with infarct-related artery patency after acute myocardial infarction

AIMS: The study was set up to evaluate the functional role of post-infarctpreserved microvascular integrity. Low dose dobutamine echocardiographyand myocardial contrast echocardiography were used to studypatients before hospital discharge who had suffered a recentmyocardial infarction and had a patent infarct-related artery(TIMI flow grade 3). METHOD: In the dysfunctioning infarct area, the wall motion score indexwas calculated at baseline, during the dobutamine infusion andat the 3 month follow-up echocardiogram; contrast echocardiographywas performed at the time of coronary angiography, before hospitaldischarge. RESULTS: In patients with more than 50% of the dysfunctioning infarctarea opacified at contrast echocardiography (group A), regionalwall motion score index decreased, compared to baseline, duringthe dobutamine infusion (1·97 ± 0·78 vs2·5 ± 0·35 at baseline; P<0·001)and at follow-up echocardiography (1·83 ± 0·63vs 2·5 ± 0·35 at baseline; P<0·001).In patients with less extensive microvascular integrity as revealedby contrast echocardiography (group B), regional wall motionscore index did not decrease from baseline during either thedobutamine infusion (2·73 ± 0·21 vs 2·81± 0·20 at baseline; P=ns) or at follow-up (2·81± 0·20 vs 2·81 ± 0·20 atbaseline; P=ns). CONCLUSION: In patients with post-infarct dysfunctioning myocardium buta patent infarct-related artery, microvascular integrity, asassessed by myocardial contrast echocardiography, is an indicatorof myocardial viability in terms of preserved contractile reserve,as demonstrated by dobutamine infusion and functional recoveryat follow-up.     

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.     

Effect of the addition of an abdominal hot can cardioverter/defibrillator pulse generator on the defibrillation energy requirements in a single-lead endocardial defibrillation system

AIMS: The effects of a cardioverter/defibrillator system with an electricallyactive generator can, applied without recourse to thoracotomy,have not been investigated in the abdominal position in humans.The purpose of this acute clinical study was to evaluate thedefibrillation efficacy of an abdominally positioned hot canelectrode in connection with a single lead endocardial defibrillationsystem. PATIENTS AND METHODS: Thirty consecutive patients undergoing implantation of a cardioverter/defibrillatoror pulse generator replacement were enrolled in this study.Each patient received an integrated, tripolar single-lead system.This was tested using an asymmetrical biphasic defibrillationwaveform with constant energy delivery. Defibrillation energy,peak voltage, peak current and impedance were compared betweentwo electrode configurations; (A) in this configuration thedistal right ventricular coil was negative and the proximalcoil positive; (B) in this configuration the distal right ventricularcoil was negative and the proximal coil and the abdominal hotcan (65 ccm), as common anode, were positive. Defibrillationthreshold testing started at 15 J with stepwise energy reduction(10 J, 8 J, 5 J and 3 J) until defibrillation was ineffective. RESULTS: Compared to the single-lead configuration, the abdominal hotcan configuration revealed at 17·5% reduction in defibrillationenergy requirements (8·6 J±4·3J vs 10·43J+3·9 J; P=0·041), a 15·7% reduction inpeak voltage (308·6±63 V vs 365·3V±68V;P0·003), and a 21·6% reduction in impedance (41·1±6·3vs 52·4±6·6·6; P>0·001).Peak current showed a significant increase during hot can testingof 8·2% (7·2 A+1·8 A vs 7·8 A±2·2A; P=0·16). CONCLUSIONS: An abdominally placed hot can pulse generator lowered defibrillationenergy requirements in patients with an endocardial defibrillationlead system.     

QT interval dispersion as a predictor of arrhythmic events in congestive heart failure: Importance of aetiology

Aims Identification of patients with congestive heart failure atrisk of sudden death remains problematic and few data are availableon the prognostic implications of QT dispersion. We sought toassess the predictive value of QT dispersion for arrhythmicevents in heart failure secondary to dilated cardiomyopathyor ischaemic heart disease. Methods and Results Twelve-lead ECGs calculated for QT dispersion, 24h Holter ECGsand signal-averaged ECGs were prospectively recorded in 205heart failure patients in sinus rhythm. The 86 patients withischaemic heart disease and the 119 with dilated cardiomyopathywere not significantly different as regards NYHA grades (51vs 49% in grades III–IV), cardiothoracic ratio (57±7vs 57±6%) and ejection fraction (28±8 vs 29±9%).The mean QT dispersion (66±29 vs 65±27ms), thefrequency of non-sustained ventricular tachycardia (37 vs 38%)and ventricular late potentials (41 vs 40%) were not significantlydifferent in patients with ischaemic or dilated cardiomyop-athy.QT dispersion was not significantly related to other arrhythmogenicmarkers. During follow-up (24±16 months), 66 patientsdied, 22 of them died suddenly and seven presented a spontaneoussustained ventricular tachycardia. In patients with dilatedcardiomyopathy, in multivariate analysis, only a QT dispersion>80ms was an independent predictor of sudden death (RR: 4·9,95% CI 1·4–16·8,P<0·02) and arrhythmicevents (RR: 4·5, 95% CI 1·5–13·5,P<0·01).In patients with ischaemic heart disease, no studied parameterwas found significantly related to sudden death or arrhythmicevents. Conclusion: In congestive heart failure, abnormal QT dispersion can identifypatients with dilated cardiomyopathy who are at high risk ofarrhythmic events.     

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.     

Sex-related differences in eligibility for reperfusion therapy and in-hospital outcome after acute myocardial infarction

AIMS: To determine the effect of sex on reperfusion therapy and earlymortality after acute myocardial infarction. MEHTODS: We analysed the characteristics, the reperfusion interventions,and in-hospital mortality in 400 consecutive patients (320 menand 80 women) admitted during the first 6 h of acute myocardialinfarction and treated by primary angioplasty, or intravenousthrombolysis with rescue angioplasty. RESULTS: The differences between men and women were age (57 vs 67 years,P=0·001), systemic hypertension (33 vs 50%, P=0·02),cigarette smoking (79 vs 30%, P=0·0001) and contraindicationsto thrombolysis (28·5 vs 42·5%, P=0·02).Successful reperfusion of the infarct-related artery was achievedin 84% of patients of both sexes. In-hospital mortality was7·2% in men and 18·7% in women (P=0·001).Multivariate analysis was performed by linear logistic regressionin order to compare several embedded models, using repeatedmaximum likelihood ratio tests. The best model involved thevariables of cardiogenic shock and age. Addition of the variable‘sex’ did not improve the predictive power of thismodel (P<0·5). CONCLUSIONS: During acute myocardial infarction, similar successful earlyreperfusion rates can be achieved in men and women, despitethe lower eligibility of women for thrombolytic therapy. Althoughin-hospital mortality was higher in women than men, the bestpredictive model of mortality was the combination of age andcardiogenic shock. Therefore, sex does not appear to be an independentpredictor of mortality.     

Relationship between haemodynamics and morphology in pulmonary hypertension: A quantitative intravascular ultrasound study

BACKGROUND: Intravascular ultrasound imaging of the pulmonary arteries hasbeen demonstrated to be a reliable method of quantifying vesseldiameter, luminal area and pulsatility. Simultaneous measurementof flow velocity and its response to vasodilators allows therelationship between morphology and functional compromise tobe studied, especially endothelial dysfunction. METHODS: In 51 patients (mean age=49·8±12·6 years,17 female) we performed right heart catheterization and simultaneousintravascular ultrasound of pulmonary artery branches. The patientswere divided in two groups: group 1 with normal pulmonary arterypressure and pulmonary vascular resistance, and group 2 withpulmonary hypertension (peak pulmonary artery pressure >30mmHg and/or mean pulmonary artery pressure >20 mmHg). Vesselwall and lumen were studied using a 2·9 F intravascularultrasound catheter with a 30 MHz phased array transducer. Measurementof blood flow velocity was accomplished by a Doppler flow wire(0·018 inch). The maximal flow change during acetylcholineinfusion (adjusted to 10^–6; 10^–5, and 10^–4Mconcentration in the blood vessel) was measured. RESULTS: There were no significant differences between groups 1 and 2with respect to age (48·5±14·3 years vs50·3±12·3 years; P=ns), gender (4 female/8male vs 13 female/26 male; P=ns), luminal area of the vesselsegment in which the intravascular ultrasound measurements wereobtained (11·8±6·1 mm² vs 16·7±14·3mm²; P=ns), internal diameter (3·9±1·2mm vs 4·2±1·7 mm; P=ns), and external diameter(6·1±1·3 mm vs 6·9±2·1mm; P=ns). Cross-sectional images of the pulmonary artery walldemonstrated a single ring with high echodensity with a thininner layer regarded as intima in group 1. In contrast, themajority of patients (n=35/39) in group 2 demonstrated a thickeningof the intimal layer and/or a disturbance of layering of theechogenic arterial wall. The relative wall thickness was higherin group 2 than in group 1 (22·5±10·4%vs 15·3±6·5% P<0·05). There wereno significant correlations between pulmonary artery pressureand wall thickness pulmonary artery pressure and area changein the cardiac cycle, acetylcholine-dependent increase in pulmonaryflow and morphological changes in the vessel wall. CONCLUSION: We conclude that intravascular ultrasound is capable of detectingmorphological changes in the pulmonary vessel wall in pulmonaryhypertension and that vessel wall hypertrophy of small pulmonarysegment arteries, as detected by intravascular ultrasound, isnot predictive of functional vasodilatory response of resistancevessels of the same vessel area.     

Effects of percutaneous balloon mitral valvuloplasty and exercise training on the kinetics of recovery oxygen consumption after exercise in patients with mitral stenosis

Aims Kinetics of recovery oxygen consumption after exercise playsan important role in determining exer-cise capacity. This studywas performed to assess the kinetics of recovery oxygen consumptionin mitral stenosis and evaluate the effects of percutaneousballoon mitral valvuloplasty and exercise training on the kinetics. Methods and Results Thirty patients with mitral stenosis (valve area 1·0cm²)and same sized age- and size-matched healthy volunteers wereincluded for this study. All subjects performed maximal uprightgraded bicycle exercise. Thirty consecutive patients who underwentsuccessful percutaneous balloon mitral valvuloplasty (valvearea 1·5cm²and mitral regurgitation grade 2), were randomizedto an exercise training group or non-training group. The exercisegroup performed daily exercise training for 3 months. Half-recoverytime of peak oxygen consumption was significantly delayed inmitral stenosis as compared to normal subjects (120±42svs 59±5,P<0·01). Peak oxygen consumption (ml.min^–1.kg^–1)was significantly increased in both the training (16·8±4·9to 25·3±6·9) and non-training groups (16·3±5·1to 19·6±6·0) 3 months after percutaneousballoon mitral valvuloplasty. Half-recovery time of peak oxygenconsumption was significantly shortened in the training group(124±39 to 76±13,P<0·01), but not inthe non-training group (114±46 to 109±44s,P=0·12)at 3 months follow-up. The degrees of symptomatic improvementafter percutaneous balloon mitral valvuloplasty were more closelycorrelated with the changes of the half-recovery time of peakoxygen consumption than those of peak oxygen consumption. Conclusion Kinetics of recovery oxygen consumption was markedly delayedin mitral stenosis, which was improved after exercise trainingbut not after percutaneous balloon mitral valvuloplasty alone.These results suggest that adjunctive exercise training maybe useful for improvement of recovery kinetics and subjectivesymptoms after percutaneous balloon mitral valvuloplasty.