Left bundle branch block: prevalence, incidence, follow-up and outcome

In a randomly selected population screening study of 8450 menand 9039 women 33 to 71 years of age conducted in Iceland in1967–1977, 27 men and 17 women were found to have leftbundle branch bock (LBBB). The prevalence of LBBB at that timewas 0.43% for men and 0.28% for women. The incidence of LBBBwas 3.2 per 10 000 per year for men and 3.7 per 10 000 per yearfor women.All except one of 37 alive patients with LBBB wereexamined in 1984 including chest X-ray, echocardiography andexercise testing (Bruce protocol). Eight men had had myocardialinfarction (P<0.05), 12 had angina pectoris, 15 had hypertension,7 had cardiomyopathy, 13 had primary conduction disease, and3 had pacemakers. Five men and two women had died in comparisonwith 18 men and 1 woman in an age-matched control group of 176people (P ns). Three of 5 decreased LBBB men had cardiomyopathyat autopsy. Three men died suddenly. The two women died of noncardiaccauses. Only one patient in the control group had cardiomyopathy(P< 0.01). There was no significant difference in other cardiacdiagnoses between the groups. Eleven LBBB women out of thirteenhad a normal exercise duration (6 min) and 11/17 men exercisednormally (7 min). In comparison with the control group, theLBBB patients had an increased LV diameter 2.85±0.38vs 2.58±0.38 cm m^-2 body surface area (P<0.01). Therewas no difference between the groups in left atrial diameteror LV wall thickness.In conclusion, the prevalence of LBBB was0.43% for men and 0.28% for women of middle age. The incidencewas 3.2 per 10 000 per year for men and 3.7 per 10 000 per yearfor women. The prognosis of LBBB is relatively benign apartfrom its association with dilated cardiomyopathy. Few patientsrequire pacemakers. The mean LV diameter is increased in randomlyselected patients with LBBB, but only those with an underlyingdisorder.     

Autonomic balance in patients with angina and a normal coronary angiogram

The pathophysiology of angina pectoris in patients with a normalcoronary angiogram is not clear. Furthermore, the pathophysiologicalimpact of ST changes in syndrome X is controversial. The purposeof this study was to investigate cardiac autonomic function,by measuring 24 h heart rate variability, in patients with andwithout electrocardiographic evidence of ischaemia during exercise. Thirty-two patients with angina pectoris, a normal coronaryangiogram, echocardiogram, hyperventilation test and gastro-oesophagealinvestigation were studied. Fourteen healthy subjects servedas controls. Fifteen patients had significant ST segment depressionduring stress testing, whereas 17 had no electrocardiographicsigns of ischaemia. Heart rate variability was calculated as(1) mean RR= mean of all normal RR intervals, (2) the differencein mean RR level between when awake and when asleep (mean RRwake-sleep)—a tentative index of sympathetic activation,(3) the standard deviation (SD)—a broad band measure ofautonomic balance, and (4) a percentage of successive RR intervaldifferences 6% (pNN6%)—an index of vagal modulation. Thecoronary vascular resistance was measured at rest and duringpacing. Mean RR and autonomic indexes did not differ between patientswith a positive exercise test and controls (831/884 m 24 h SD125/134 m pNN6% 6.715.4%, respectively). Patients with a normalexercise test had shorter mean RR (758 ms vs 844 m P<0.05)and significantly reduced 24-h SD (103 ms vs 134 m P<0.05)than controls, whereas values for vagal index (6.5% vs 5.4%)did not differ from healthy controls. Mean RR wake-sleep alsotended to be lower in patients with a normal exercise test (–125 ms vs – 173 ms) compared to controls (P<0.1). Patientswith a positive exercise test had a significantly attenuatedreduction in coronary vascular resistance during pacing in comparisonto patients with a normal exercise test (–0.131–0.26mmHg x min. ml^{– 1}; P<0.05). The findings suggest the occurrence of general elevated sympatheticactivation in angina patients with a normal exercise test. Patientswith a positive exercise test exhibited no signs of autonomicdysfunction although these patients had altered coronary vascularresistance indicating microvascular angina. This supports thesuggestion that patients with a normal exercise test constitutean independent pathophysiological entity.     

Lack of correlation between haemodynamic and cardiopulmonary exercise capacity improvement after catheter-balloon mitral valvuloplasty

The long-term effects of percutaneous transvenous mitral commissurotomyon exercise capacity and ventilation were investigated to determinewhether a dissociation between haemodynamic improvement andexercise capacity increase occurs in patients with mitral stenosis.Eighteen patients aged 45 ± 12.3 years (mean ±SD) with symptomatic mitral stenosis performed a symptom-limitedbicycle exercise test while respiratory gases were measuredbefore and 6 months after percutaneous transvenous mitral commissurotomy.The mitral valve area increased from 1.07 ±0.22 to 1.98±0.67 cm². P<0.0001 and the mean mitral gradient decreasedfrom 12.9 ±4.5 to 5.3±4.8mmHg, P<0.001, withouta significant increase in cardiac output index (from 2.64 ±0.55 to 2.77 ± 0.56 l. min_{– 1}. m_{– 2}, P= ns).This haemodynamic improvement was still present at the 6-monthfollow-up catheterization. Mean exercise workload and peak oxygenuptake increased 6 months after percutaneous transvenous mitralcommissurotomy from 88.3 ± 28.1 to 97.8 ± 25.1watts, P= 0.01, and from 18.1 ± 5.3 to 19.9 ±4.8 ml. kg_{– 1}.min_{– 1}, P<0.05. Total ventilation,ventilatory equivalents and oxygen pulse at the end of the exercisetest remained unchanged Correlations between peak oxygen orexercise capacity improvement and mitral valve area increasewere poor (r= 0.27, P= ns, r= 0.24, P=ns). This clear dissociationbetween haemodynamic improvement and improvements in minor exercisecapacity after percutaneous transvenous mitral commissurotomysuggests that peripheral alterations persist. Future studiesin which patients are trained after valvuloplasty may be helpful.     

Inferior ST segment depression as a useful marker for identifying proximal left anterior descending artery occlusion during acute anterior myocardial infarction

To determine whether or not ST segment deviation on admissionelectrocardiograms can identify patients with anterior acutgemyocardial infarction due to proximal left anterior descendingartery occlusion, the magnitude and location of ST segment elevationor depression were compared between patients with proximal leftanterior descending artery occlusion (group A, n=47) and thosewith distal left anterior descending artery occlusion (groupB, n =59). ST segment depression in each of the inferior leadswas significantly greater in group A than in group B. The incidenceof ST segment depression 1 mm in each of the inferior leads(II; 81% vs 27%, III; 85% vs 54%, aVF; 87% vs 47%, P<0·01)was significantly higher in group A than in group B. In addition,the incidence of ST segment depression 1 mm in all of the inferiorleads was significantly greater in group A than in group B (77%vs 22%, P<0·01). In group A, maximal ST segment elevationwas more frequent in lead V alone (43% vs 14%, P<0·01).Group A had greater ST segment elevation in lead a VL than groupB, and the incidence of ST segment elevation 1 mm in lead aVL was significantly higher in group A than in group B (66%vs 47%, P<0·05). ST segment depression 1 mm in allof the inferior leads was most valuable for identifying groupA patients (77% sensitivity and 78% specificity). In contrast,the maximal ST segment elevation in lead V₂ alone or ST segmentelevation 1 mm in lead a VL had a low diagnostic value (43%sensitivity and 86% specificity, 66% sensitivity and 53% specificity,respectively). In conclusion, this study indicates that analysisof ST segment deviation in the inferior leads is useful foridentifying patients with acute anterior myocardial infarctiondue to proximal left anterior descending occlusion.     

Determination of left ventricular wall thickness and muscle mass by intravenous digital subtractionangiocardiography: validation of the method

Left ventricular (LV) wall thickness and muscle mass are importantmeasures of LV hypertrophy. In 24 patients LV end-diastolicwall thickness and muscle mass were determined (two observers)by digital subtraction angiocardiography (DSA) and conventionalLV angiocardiography (LVA). Wall thickness was determined overthe anterolateral wall of the left ventricle according to thetechnique of Rackley (method 1) or by planimetry (method 2).Seventeen patients were studied at rest and seven during dynamicexercise. Wall thickness correlated well between LVA and DSA;the best correlations were obtained by a combined subtractionmode using either method 1 or 2 (method 1, r0–80; method2,r0. 75). The standard error of estimate of the mean (SEE) wasslightly lower for method 2 ( 10%) than for method 1 ( 13%).DSA significantly overestimated wall thickness by 5–7%with method 1 and underestimated by 12–14% with method2. Muscle mass correlated well between LVA and DSA; the SEEwas 15% for method 1 and 12% for method 2. Overestimation ofmuscle mass by DSA was 7–11% with method 1 and underestimationwas 13–15% with method 2.It is concluded that LV wallthickness can be determined accurately by DSA with an SEE rangingbetween 10 and 13%. Determination of LV muscle mass is slightlyless accurate and the SEE is slightly larger ranging between13 to 17%. With method 1, wall thickness and muscle mass wereover estimated and with method 2 underestimated.     

Increased mortality in men with ST segment depression during 24 h ambulatory long-term ECG recording: Results from prospective population study 'Men born in 1914', from Malmo Sweden

‘Men born in 1914’, from Malmö, Sweden, isa cohort study of the morbidity and mortality of cardiovasculardiseases among 68-year-old men in an urban population. Ambulatorylong-term ECG recording was part of the health examination thatthese men were invited to undergo in 1982. Five hundred attended(80.5%) of the 621 invited. Ninety-eight of the 394 men in whomthe ECG recording was technically satisfactory had at leastone episode with horizontal or down sloping ST segment depression0.1 mV. The median total duration of ST segment depression was135 min. 90% of these episodes were not preceeded by any increasein heart rate. In only eight of the 47 men who reported an occurrenceof chest symptoms during the recording period did ST segmentdepression and chest symptoms occur simultaneously. 43 monthsafter the health examination, 33 (8.4%) men had died. The mortalityin men without ST segment depression and without any historyof coronary heart disease was 6.5%. The incidence of fatal andnon-fatal myocardial infarction in men without ST depression0.l mV and without a history of IHD was 2.3%. Men with ST depression0.1 mV in comparison with this group had a 4.4 times greaterrelative risk. The risk in men with both ST segment depression0.1 mV and history of coronary heart disease was 16.0 timesgreater. This study shows that asymptomatic ST segment depressionis a frequent finding in elderly men. The occurrence of asymptomaticST segment depression is associated with an increased cardiovascularmortality. This increased mortality is independent of a historycompatible with angina pectoris or previous myocardial infarction.     

Time domain analysis of the signal averaged electrocardiogram in patients with a conduction defect or a bundle branch block

Doubts have been expressed about the clinical usefulness oftime domain analysis of the signal averaged electrocardiogramin patients with prolonged QRS complex duration. We studied147 patients using a signal averaged ECG (40–250 Hz) whoseQRS complex was longer than 100 ms. A baseline electrophysiologystudy was also performed in 128 of these patients. Seventy-sevenpatients had a minor (QRS <120 and >100 ms) conductiondefect. Thirty-seven of these 77 had either induced or spontaneoussustained ventricular tachycardia (group I) and 40 had no sustainedventricular tachycardia (group II). Seventy patients had a major(QRS120 and >100 ms) conduction defect, 44 of whom had sustainedventricular tachycardia (group A). The remaining 26 withoutthis condition formed Group B. Group I compared to group IIpatients had a longer filtered QRS duration (120·8 ±14 vs 104·5 ± 9·5 ms, P<0·001),a longer low amplitude signal duration (41 ± 12·1vs 31 ± 12·6 ms, P<0·0001) and a lowerroot mean square of the last 40 ms of the filtered QRS complex(27 ± 29·8 vs 35 ± 25·3 µV,P=ns). Group A compared to group B had a longer filtered QRSduration (157·7±20·2 vs 140·7±15·7 ms, P<0·001), a longer low amplitude signalduration (57·3 ±24·9 vs 37·8 ±20·3 ms P<0·001) and a lower root mean squareof the last 40 ms of the filtered QRS complex (14·3 ±11·2 vs 22·0 ± 10·5 1 P<0·01).Using conventional late potential criteria, the sensitivityand specificity of the signal averaged ECG for the detectionof sustained ventricular tachycardia patients with a minor conductiondefect were 89% and 75%, respectively. The same criteria appliedto patients with a major conduction defect were sensitive (sensitivity:87%) but non-specific (specificity: 50%). However, by usingmodified late potential criteria, such as the presence of twoof any of the following three signal averaged parameters: filteredQRS duration 145 ms, low amplitude signal duration 50 ms,root mean square of the last 40 ms of the filtered QRS complex17·5µV, we derived a non-optimal but still acceptablecombination of sensitivity (68%) and specificity (73%). We concludethat traditional late potential criteria can be applied in patientswith a minor conduction defect, but modification of these criteriais necessary to derive useful clinical information for riskstratification of patients with a QRS complex duration 120ms.     

Differences in restenosis propensity of devices for transluminal coronary intervention: A quantitative angiographic comparison of balloon angioplasty, directional atherectomy, stent implantation and excimer laser angioplasty

With the increasing clinical application of new devices forpercutaneous coronary revascularization, maximization of theacute angiographic result has become widely recognized as akey factor in maintained clinical and angiographic success.What is unclear, however, is whether the specific mode of actionof different devices might exert an additional independent effecton late luminal renarrowing. The purpose of this study was toinvestigate such a difference in the degree of provocation ofluminal renarrowing (or ‘restenosis propensity’)by different devices, among 3660 patients, who had 4342 lesionssuccessfully treated by balloon angioplasty (n=3797), directionalcoronary atherectomy (n= 200), Palmaz-Schatz stent implantation(n= 229) or excimer laser coronary angioplasty (n= 116) andwho also underwent quantitative angiographic analysis pre- andpost-intervention and at 6-month follow-up. To allow valid comparisonsbetween the groups, because of significant differences in coronaryvessel size (balloon angioplasty=2.62±0.55 mm, directionalcoronary atherectomy= 3.28±0.62 mm, excimer laser coronaryangioplasty= 2.51±0.47 mm, Palmaz-Schatz=3.01±0.44mm;P<0.0001), the comparative measurements of interest selectedwere the ‘relative loss’ in luminal diameter (RLoss=losslvessel size) to denote the restenosis process, and the‘relative lumen at follow-up’ (RLfup=minimal luminaldiameter at follow uplvessel size) to represent the angiographicoutcome. For consistency, lesion severity pre-intervention was representedby the ‘relative lumen pre’ (RLpre=minimal luminaldiameter prelvessel size) and the luminal increase at interventionwas measured as ‘relative gain’ (relative gain=gainl vessel size). Differences in restenosis propensity betweendevices was evaluated by univariate and multivariate analysis.Multivariate models were constructed to determine relative lossand relative lumen at follow-up, taking account of relativelumen pre-intervention, lesion location, relative gain, vesselsize and the device used. In addition, model-estimated relativeloss and relative lumen at follow-up at given relative lumenpre-intervention relative gain and vessel size, were comparedamong the four groups. Significant differences were detectedamong the groups both with respect to these estimates, as wellas in the degree of influence of progressively increasing relativegain, on the extent of renarrowing (relative loss) and angiographicoutcome (relative lumen at follow-up), particularly at higherlevels of luminal increase (relative gain). Specifically, lesionstreated by balloon angioplasty or Palmaz-Schatz stent implantation(the predominantly ‘dilating’ interventions) wereassociated with more favourable angiographic profiles than directionalatherectomy or excimer laser (the mainly ‘debulking’interventions). Significant effects of lesion severity and location,as well as the well known influence of luminal increase on bothluminal renarrowing and late angiographic outcome were alsonoted. These findings indicate that propensity to restenosis afterapparently successful intervention is influenced not only bythe degree of luminal enlargement achieved at intervention,but by the device used to achieve it. In view of the clinicalimplications of such findings, further evaluation in largerrandomized patient populations is warranted.     

Exercise training in heart failure improves quality of life and exercise capacity

Aims Benefit from exercise training in heart failure has mainly beenshown in men with ischaemic disease. We aimed to examine theeffects of exercise training in heart failure patients 75 yearsold of both sexes and with various aetiology. Methods and Results Fifty-four patients with stable mild-to-moderate heart failurewere randomized to exercise or control, and 49 completed thestudy (49% 65 years; 29% women; 24% non-ischaemic aetiology;training, n=22; controls, n=27). The exercise programme consistedof bicycle training at 80% of maximal intensity over a periodof 4 months.Improvements vs controls were found regarding maximalexercise capacity (6±12 vs –4±12% [mean±SD],P<0·01)and global quality-of-life (2 [1] vs 0 [1] units [median {inter-quartilerange}],P<0·01), but not regarding maximal oxygenconsumption or the dyspnoea–fatigue index. All of thesefour variables significantly improved in men with ischaemicaetiology compared with controls (n=11). However, none of thesevariables improved in women with ischaemic aetiology (n=5),or in patients with non-ischaemic aetiology (n=6). The trainingresponse was independent of age, left ventricular systolic function,and maximal oxygen consumption. No training-related adverseeffects were reported. Conclusion Supervised exercise training was safe and beneficial in heartfailure patients 75 years, especially in men with ischaemicaetiology. The effects of exercise training in women and patientswith non-ischaemic aetiology should be further examined.     

Observations of the relationship between left ventricular aneurysm and ST segment elevation in patients with a first acute anterior Q wave myocardial infarction

Seventy-eight consecutive survivors of a first acute anteriorQ wave myocardial infarction (AMI) underwent two-dimensionalechocardiography (2D echo), colour Doppler echo and radionuclideangiography (RNA) for the diagnosis of left ventricular (LV)anteroapical aneurysm, in order to study the relationship ofthis complication to precordial ST segment elevation in thesepatients. The ST elevation (mm) in lead V₂, the maximum ST elevationin V₁-V₆ and the sum of ST elevation in V₁ to V₆ were calculated.LV aneurysm was present in 19 patients by 2D echo, of whom 12had a paradoxical systolic flow pattern (red and outward towardsthe transducer) at the apex. There was no difference between the mean ST elevation in V₂or the maximum ST elevation in V₁-V₆ in patients with and withoutan aneurysm, although the sum of ST elevations in V₁ to V₆ washigher in the former group (P<0.01). ST elevation of patientswith and without paradoxical systolic flow also did not differsignificantly. Wall motion abnormality (akinesis and dyskinesis)by 2D echo in the anterior wall was seen in 74% of patientswith and 36% of patients without an aneurysm (P<0.005), andin the septal region in 63% and 47% of respective patients (P-NS).There was no difference between the magnitude of ST elevationin subgroups of patients with ejection fraction (EF) 30% to40%, but the mean EF of patients with (23 ± 2.1%) andwithout a LV aneurysm (34 ± 1.3%) differed (P<0.001). It is concluded that precordial ST segment elevation does notclearly and in the diagnosis of an anteroapical LV aneurysm.It is related to akinesis and dyskinesis in anterior and septalregions inherent in patients with AMI and does not indicateimpaired LV function.     

Range of normal values for left and right ventricular ejection fraction at rest and during exercise assessed by radionuclide angiocardiography

In order to reach a world-wide consensus on the normal rangeof left (LV) and right ventricular (RV) ejection fraction (EF)at rest and during exercise, pooled data of 1200 normal subjectsfrom 28 leading centres in the field of nuclear cardiology (68%of those contacted) was analysed. Weighted mean normal valuesfor LVEF at rest were 62.3±6.1% (1SD) with a lower limitof normal of 50% and for RVEF 52.3±6.2% (N=365) witha lower limit of normal of 40%. During exercise, LVEF increasedin 475 subjects by +8.0 EF% (range 3–15%), a normal increasebeing accepted to be 5% over a normal resting value for bothLVEF and RVEF. Subgroup analysis of results at rest revealedno significant differences regarding selection of normal subjects(based on normal catheterization findings vs. normal volunteerswith low probability of disease), age or sex. During exercise,however, significantly larger increases in LVEF measurementswere noted for men versus women (P<0.01), for normal volunteersversus subjects selected as ‘normals’ based on anormal coronary angiogram (P<0.001) and for younger versusolder subjects (P<0.001). Data on reproducibility and variabilityshowed that radionuclide angiocardiography can be consideredto be a reliable method today. No consensus was found for measurementsof regional LV function or wall motion mainly because of differencesin methodology used. These normal values may serve as generalguidelines for future applications of these techniques but factorswhich may influence the normal range as defined and discussedin this study should be recognized.     

Detection of acute myocardial infarction by a new, sensitive and rabid method for determination of creatine kinase B-subunit activity

An immunoinhibition method for the assay of creatine kinase(CK) isoenzymes by continuous monitoring of the ATP formationin the CK reaction by a purified firefly luciferase reagenthas been developed. The sensitivity of the firefly assay ofATP makes it possible to assay CK-B subunit activity (CK-B)in serum down to 1 U/l. In healthy individuals CK-B varied between 2 and 12, mean 3U/l. A wide range of CK-B activity was observed after acutemyocardial infarction (AMI), intramuscular injection and surgerywith overlapping between these different categories. Thereforethe maximal change in CK-B activity (CK-B) was studied in 98patients admitted to a coronary care unit. In all 57 patientswithout a subsequent diagnosis of AMI according to conventionalcriteria CK-B was < 5 U/l. In all 41 patients with AMI CK-Bwas 5 U/l. In all healthy individuals CK-B was < 2 U/l.CK-B 5 U/l was found after i.m. injection and different kindsof surgery in three out of 60 patients. Thus, the present method for determination of CK activity hasbeen shown to possess high precision in low activities, to beas rapid as conventional methods and to be simple enough tobe used in a routine laboratory. With these properties the methodshould be suited for early diagnosis and early exclusion ofeven very small AMIs.     

ST segment depression in lateral limb leads in inferior wall acute myocardial infarction: Implications regarding the culprit artery and the site of obstruction

We examined whether the pattern of ST segment depression inlateral leads (I, aVL, V5, V6) in the initial electrocardiogramof patients (n=88) with inferior wall acute myocardial infarction(ST segment elevation of 1 mm in 2 inferior leads) correlateswith the site of obstruction, as determined angiographicallyduring acute hospitalization. Of the 62 patients in which the culprit artery could be determinedunequivocally, in 46 the culprit artery was the right coronaryartery (20 proximal to the first right ventricular branch and26 distal), and in 16 the left circumflex coronary artery (sevenproximal to the first marginal branch or involving a high firstmarginal branch, and nine with distal obstruction). SignificantST segment depression (ST1 mm) in leads I and aVL was more commonin right coronary artery obstruction (P<0.05 and P<0.0001,respectively). The absence of significant ST segment depressionin lead a VL was most common in proximal circumflex obstruction(P<0.0001), with a similar trend for lead I (P<0.11).ST segment depression patterns in leads V₅ and V₆ were not indicativeof the infarct-related artery or the site of obstruction. Thus,significant ST segment depression in leads I and aVL indicatesright coronary artery-associated inferior wall acute myocardialinfarction with a sensitivity of 70% and 100%, and a specificityof 63% and 38%, respectively, whereas the lack of ST segmentdepression in these leads indicates proximal circumflex obstructionwith a sensitivity of 71% and 86%, and a specificity of 65%and 100%, respectively.     

Protective effect of beta-blockade on dipyridamole-induced myocardial ischaemia: Role of heart rate

This study was designed to investigate the effect of heart ratechanges on dipyridamole echocardiographic tests in patientswith coronary artery disease treated with propranolol. We prospectively studied 12 patients (8 men and 4 women; meanage 56.5 ± 8.7 years) selected by: (a) angiographic evidenceof significant coronary artery disease; (b) adequate echocardiographicwindow; (c) positive dipyridamole echocardiography test resultsin baseline conditions (step I); (d) test reproducibility inthe absence of treatment; (e) negative dipyridamole echocardiographytest results after 7 days of treatment with propranolol (120mg. day^–1) in twice divided doses daily (step II). In all patients treated with propranolol, dipyridamole echocardiographictesting was repeated 24 h after the last negative test. In thesepatients, transoesophageal atrial pacing was performed at peakdipyridamole infusion to increase heart rate to values similarto those observed at baseline (step III). At baseline, heartrate and rate-pressure product were significantly lower in patientstreated with propranolol (–20.3% and –22.5% in groupII, P<0–001 vs step I; –24.3% and –26.4%in group III, P<0.05 vs step I), but the different treatmentsdid not produce significant differences in systolic and diastolicblood pressure. At peak dipyridamole infusion, heart rate andrate-pressure product increased with either placebo or propranololtreatments with respect to baseline, while remaining significantlylower with propranolol as compared to placebo ( –29.6%and –29.5% in step II, P<0001). During treatment withpropranolol plus transoesophageal pacing to maintain heart rateat values attained with placebo, the rate-pressure product didnot change significantly with respect to placebo, nor did systolicblood pressure. Transoesophageal atrial pacing performed duringpropranolol treatment to restore heart rate to baseline valuesdid not affect the dipyridamole echocardiographic test in eightpatients (group I), and induced transient wall abnormalitiesin four patients (group II) (P=ns). Our data suggest that the anti-ischaemic effect of propranololin man is not correlated only to reduction of heart rate.     

Doppler echocardiography in adults with isolated ventricular septal defect

Doppler echocardiography and cardiac catheterization were undertakenin 70 consecutive patients, 31-68 years of age (mean 39), whohad isolated congenital ventricular septal defects (VSD), 28of whom had been operated upon. In 50 patients with invasivelyproven VSD, 37 had a correct Doppler diagnosis of VSD (group1) and in 13 a false negative result was obtained (group 2);i.e. a sensitivity of 74%. No false positive Doppler diagnosiswas made in the 20 patients without evidence of shunt. Leftto right ventricular systolic pressure difference (P) rangedbetween 55 and 142 mm Hg, with a mean value of 103 mm Hg ingroup 1 and 99 mm Hg in group 2. There was good correlationbetween P obtained by continuous wave Dopier and catheterisationin 17 group 1 patients with moderate and large shunts (r=0.81,P<0.001). There was no correlation in the remaining 20 patientsin group 1 with small shunts (r=0.20, P>0.l). Doppler echocardiography in the adult with isolated VSD hasgood sensitivity and excellent specificity. Doppler predictionof P is reasonably correct in patients with moderate and largeshunts, but of no value in patients with small shunts.     

Haemodynamic findings in experimental right ventricular ischaemia after right coronary arterial ligation

Acute ischaemia limited to the free wall of the right ventriclewas produced by right coronary arterial ligation (RCAL) in 20dogs. Contrast M-mode and cross-sectional echocardiography wasperformed in 7 cases to investigate the presence of tricuspidinsufficiency. The haemodynamic findings obtained with an openpericardium at 15 to 30 min showed increases in right (l.20.5to 2.70.7 mmHg, P0.01) andleft (5.0 0.8 to 6.60.9 mmHg, P005)ventricular end-diastolic pressures, and decreases in heartrate (1394.9 to 1195.1 bpm, P0.01), cardiac index (1066.6 to817.3 ml min^–1 kg^–1, P001), stroke index (79 6 to72 8 ml x 100 beat^–1 kg^–1, P0.02), right (23.8l.5to 19.41.5 mmHg, P0.01) and left (1097.2 to 958.2 mmHg, P005)ventricular systolic pressures and right ventricular strokework index (18.32.4 to 11.41.8 g m kg^–1, P0.01). In 6of 15 cases the 'y' descent became deeper than the 'x' descentin right atrial pressure (RAP). Tricuspid insufficiency gradeI–II/IV was present in 3 of 7 cases, 2 of them with a'y'>'x' in RAP. Right ventricular mechanical alternans, probablysecondary to a decrease in contractility, appeared in 10 of20 cases after RCAL. Closure of the pericardium exaggeratedthe haemodynamic alterations and a dip-plateau appeared in 2cases on the right ventricular pressure curve. We conclude thatsignificant aemodynamic alterations in right ventricular functionare produced by RCAL in dogs, and they are exaggerated afterclosing the pericardium.     

Blunted humoral responses to mental stress and physical exercise in cardiac transplant recipients

Since recent results have suggested that the relative neuroendocrineresponse to physical activity is exaggerated following cardiactransplantation, we studied the haemodvnamic-neuroendocrineresponses to mental stress, and to physical exercise, in hearttransplant recipients free of antihypertensive medication. Tenpatients were studied 17 years (mean) after transplantationand compared with 10 age-matched controls. Plasma levels ofcatecholamines, renin activity, aldosterone, atrial natriureticfactor, calcitonin gene-related pep tide (CGRP), and endothelinwere measured, together with blood pressure and heart rate,during mental stress and graded, submaximal ergometry. Mental stress increased blood pressure in both groups (P<0·02),but heart rate in controls only (P<0.05). Noradrenaline didnot change. Adrenaline rose in controls only (P<005). Plasmarenin activity increased in both groups (P<0.02), while aldosteroneincreased in controls only P<0.02). A trial natriuretic factor,and endothelin were higher in patients (P <0.01). Mentalstress, however, did not induce any changes. No signficant differenceswere found in relative changes (% except for plasma renin activitywhich was greater in controls (P<0.05). During ergometry,only % noradrenaline was greater in patients (P<0.05). %for all other parameters were either of tile same order as incontrols, or blunted. Thus, apart from noradrenaline, cardiactransplant recipients, not receiving antihypertensive medication,do not show an exaggeration in the relative neuroendocrine responseto mental or physical stress.     

Good exercise capacity at hospital discharge predicts recovery of baroreflex sensitivity after myocardial infarction

Myocardial infarction results in depressed baroreflex sensitivity,which has been shown to be associated with increased risk ofventricular arrhythmias and sudden death. We measured baroreflexsensitivity in 37 patients with acute myocardial infarctionbefore hospital discharge and 3 months after the infarctionto find out whether the baroreflex sensitivity recovers duringthat period. In addition, baroreflex sensitivity was assessedin 15 healthy controls. Baroreflex sensitivity was assessedfrom the regression line relating the change in R-R intervalto the change in systolic blood pressure following an intravenousbolus injection of phenylephrine. There was a wide inter-individualvariation in the change of baroreflex sensitivity (Abaroreflexsensitivity) in infarction patients, but the average baroreflexsensitivity showed no significant change during the 3-monthfollow-up (10.2 +5.6 to 11.8 ± 7.5 ms. mmHg ^–1,ns) and remained lower than the baroreflex sensitivity of thecontrols (16.4 ± 9.7 ms. mmHg^–1, P<0.05). Baroreflexsensitivity correlated significantly with exercise capacitymeasured before hospital discharge. When the patients were dividedinto tertiles according to the baroreflex sensitivity ( –3.3 ± 1.5 ms. mmHg^–1 in the lowest tertile, 1.0± 1.0 ms. mmHg^–1 in the middle tertile and 7.5± 40 ms. mmHg^–1 in the highest tertile) the exercisecapacity was found to increase from the lowest to the highesttertile (exercise time 357 ± 115 s, 418 ± 126s and 461 ± 141 s, respectively; P<0.05 lowest vshighest tertile). Patients with a low exercise tolerance (exercisetime <360 s) showed a significantly smaller Abaroreflex sensitivitythan patients with a good exercise tolerance (exercise time480s) ( – 0.5±4.4 vs 5.3 ± 5.4ms. mmHg^–1,P<0.05), respectively. Baroreflex sensitivity was not relatedto the location or type of infarction, thrombolytic therapy,presence of angina pectoris or left ventricular function atthe time of discharge. In conclusion, exercise capacity assessedbefore hospital discharge seems to be a predictor of baroreflexsensitivity recovery in patients with a recent myocardial infarction.     

Biplane transoesophageal echocardiography, transthoracic Doppler, and magnetic resonance imaging in the assesment of coarctation of the aorta

This study compared flow-sensitive magnetic resonance imagingwith biplane transoesophageal echocardiography in combinationwith continuous wave Doppler from the suprasternal notch inpatients with native coarctation or after surgical repair. Twenty patients (mean age 33 years, range 17–60) wereinvestigated, of whom 15 had undergone surgery at mean age 13years, range 5.43. Peak and mean flow in the ascending and descendingaorta as well as coarctation peak velocity were determined withthe magnetic resonance imaging phase contrast technique. Coarctationpeak velocity was also measured by Doppler from the jugulum.Magnetic resonance imaging axial sections as well as biplanetransoesophageal echocardiography were used to measure the smallestdiameter of the constricted segment. Sixteen healthy volunteers,mean age 36 years, range 22.63, provided reference values formagnetic resonance imaging determined volume of flow in theaorta. Peak flow in the descending aorta was 9.2 ±3.71.min ^{– 1} (reference 130 ± 2.5, P<0.01) and meanflow 3.1 ±0.9 I. min^{– 1} (reference 3.4 ±0.8,P>0.05). The ratio of descending-to-ascending peak flow was0.54 ±0.17 (reference 0.69 ± 0.10, P<0.01)and mean flow 0.68 ± 0.15 (reference 0.69 ± 0.08,P>0.05). The coarctation velocity was slightly higher withDoppler than with magnetic resonance imaging (+ 0.24 ±0.44 m. s^{– 1}, 95% confidence interval +0.45 to + 0.02m.s^{– 1}, P= 0.05). The coarctation diameter was slightlylarger with magnetic resonance imaging than with transoesophagealechocardiography (1.4 ±3.5 mm, 95% confidence interval+ 3.1 to – 0.3 mm, P= 0.11). Both methods are suitable for the assessment and follow-up ofcoarctation of the aorta Flow assessment with magnetic resonanceimaging provides a hitherto unavailable measure with which toassess the severity of obstruction.     

Sex-dependent differences in left ventricular function and structure in chronic pressure overload

To evaluate gender-related differences in left ventricular (LV)structure and function in aortic stenosis, LV biplane cineangiography,micromanometry and endomyocardial biopsies were carried outin 56 patients with aortic stenosis and normal coronary arteries.Patients were divided into males (M: n=35), and females (F:n=21). Sixteen normal subjects 8 M, 8 F) served as haemodynamiccontrols. Control biopsy data were obtained from six pre-transplantationdonor hearts (3 M and 3 F). LV systolic function was evaluatedby ejection fraction and its relationship to mean systolic circumferentialwall stress, diastolic function by the time constant of LV pressuredecay, peak filling rates and passive myocardial stiffness constant.Biopsy samples were evaluated for interstitial fibrosis, musclefibre diameter and volume fraction of myofibrils. In a subsetof 27 consecutive patients, biopsy samples were evaluated witha morphometric-morphological method, for total collagen volumefraction, endocardial fibrosis and the extension and thicknessof orthogonal collagen fibres (cross-hatching). In patients with aortic stenosis, aortic valve area, aorticvalve resistance and mean aortic pressure gradient were comparablein males and females, whereas end-systolic and end-diastolicvolumes were larger in males than females. Ejection fractionwas lower (56%) in males than females (64%) (P<0.05); 20of 35 males and four of 21 females had depressed systolic contractilitywhen assessed with regard to the relationship ejection fraction-meansystolic stress (P<0.01). Myocardial stiffness constant washigher in males than in females (P<0.0I). Nine of 14 malesand two of 13 females had endocardial fibrosis (P<0.009),whereas increased cross-hatching (> 1.5 grade) was presentin 11 males and four females with aortic stenosis (P<0.0I).An abnormal collagen architecture was present in 13114 malesand 5113 females (V<0.002). In aortic stenosis, males have a depressed systolic functionand abnormal passive elastic properties when compared to femaleswith valve lesions of similar severity. Changes in collagenarchitecture may account, at least in part, for these differences.