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.     

Right and left ventricular ejection fraction and left ventricular volume changes at rest and during exercise in normal subjects

The effect of exercise upon right and left ventricular ejectionfractions (RVEF and LVEF) as well as the changes upon left ventricularend-diastolic and end-systolic volume indices (LVEDVI and LVESVI)were investigated. Twenty-two normal subjects were studied atrest and during upright submaximal exercise. RVEF was determinedusing a first-pass method. LVEF was measured using multiplegated blood pool imaging. During the exercise test ECGs remained normal. HR and BP increasedsignificantly (P<0.01). RVEF increased from 44%±4(mean±SD) to 60%±6 (P<0.001). LVEF increasedfrom 62%±6 to 76±5 (P<0.001). A wider scatterwas observed in RVEF than in LVEF. There was a 14% increasein LVEDV-index and a 14% decrease in LVESV-index (P<0.001).A multiple regression analysis with RVEF as the dependent variableand HR, systolic BP, LVEF, LVEDV-index and LVESV-index as independentvariables showed a significant correlation between RVEF andLVEF and systolic BP (P<0.05). Our data provide insight intothe mechanisms by which the pump performance is increased innormal subjects. The central mechanisms observed are the Starlingeffect and an increase in contractility of the myocardium. Thisis connected in the general circulation to an increase in afterload,indicating a redistribution of blood from the vascular bedsto the muscles and to the heart.     

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.     

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.     

Rapid diminution of calcium in the myocardium by transfer to pericardial solutions: Myocardial dialysis

A new method is described for the controlled and specific depletionof calcium from the vascularly perfused heart of experimentalanimals by means of dialysis, using a pericardial solution. A 30–40ml isotonic phosphate buffer pH7.3 with a low Ca²⁺ and high Mg²⁺ concentration (0.2 and 2.7mM respectively) wasinserted into the pericardial cavity of anaesthetized dogs andkept therefor 10 or 60 min. The calcium content of the subendocardialand subepicardial halves of the left ventricular wall was similarlydecreased to about 70% (P<0.01) within 10 min and to 62%(P<0.001) at 60 min, compared to that of hearts dialysedfor60 min in a standard solution ofCa²⁺ 1.2 mM and Mg²⁺ 1 mM.Calcium content of the myocardium dialysed with low Co²⁺ anda standard Mg²⁺ solution decreased to only 75% (P<0.01)at 60 min. Similar changes of calcium were measured in otherparts of the heart. An increase in Co²⁺ concentration in the pericardial solutionwas observed at the same time as a decrease in calcium in themyocardium. The increase in Ca²⁺ reached about 0.7 mM at 60min, but decreased slightly, and finally, fell to 85% of pre-dialysisvalues at 60 min. It is concluded that this method of myocardial dialysis is effectivein reducing myocardial calcium and is influenced by the durationof dialysis and the Mg²⁺ content of dialysate.     

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.     

Use of changes in ST segment elevation for prediction of infarct artery recanalization in acute myocardial infarction

Background: The role of the ECG in evaluating reperfusion statusafter thrombolytic treatment in acute myocardial infarctionis not clear. Dramatic ST segment changes have been observedduring recanalization of an infarct-related artery, but ST criteriahave not been definitively established for prediction of coronaryartery patency. Differences in ST segment changes in relationto infarct localization have not been evaluated, and furtherinvestigation is required into reciprocal ST depression, whichprovides information independent from ST elevation. Therefore,the aim of this study was to evaluate how early changes in STsegment elevations and depressions predict vessel patency afterfibrinolysis for patients with anterior and inferiorllateralinfarcts. Methods and Results: Two hundred patients with a Pardee wavein the ECG and chest pain of less than 6 h duration were giventhrombolytic treatment. The result of the therapy was assessedsimultaneously with coronary angiography. Patients were dividedinto two groups: I (50 patients) without recanalization (TIMIgrade 0, 1 or 2), and II (150 patients) with successful recanalization(TIMI grade 3). Before and after therapy, analysis of the 12lead ECG included maximum ST elevation measurement (H₁, H₂ respectively),the sum of ST elevations (H₁, H₂), the sum of ST segment depressions(h₁, h₂), and the ratios of ST segment changes (R₁ = H₂:H₁,R₂ = H₂:H₁, R₃ = h₂:h₁). The mean interval from the first tothe second ECG was 3.5 ± 1 h. Successive values of R₁and R₂ were examined to find that which best distinguished betweenthe two groups. The best values for prediction of reperfusionwere: (1) For anterior wall infarct Specificity Sensitivity R₁ 0.6 83.3% 88.7% R₂ 0.5 83.3% 92.0% (2) For inferior and lateral infarct R₁ < 0.5 100% 93.8% R₂ < 0.5 100% 92.8% In 13 patients with a complete right or left bundle branch blockin the first or second ECG, the result of treatment was predictedin 11 patients using criteria for factor R₁ and in 12 patientsusing criteria for R₂ Analysis of ST segment depressions revealed a significant correlationbetween normalization of ST segment depressions and elevations(R₃ vs R₁: r = 0.60, P < 0.05; R₃ vs R₂ r = 0.59, P <0.05). Multivariate discriminant analysis showed an independentvalue of R₃for discrimination between the two groups, but onlyin patients with inferiorllateral infarcts. The overall accuracyof the common algorithm in predicting reperfusion was significantlybetter in patients with inferiorllateral infarcts (Chi² test,P = 0.0078). When separate algorithms were used, there was nosignificant difference between patients with anterior or inferiorllateralinfarcts because of the significant improvement in predictionof reperfusion in patients with anterior infarcts (McNemar'stest: P = 0.041). Conclusions: We conclude that analysis of ST segments on thestandard 12-lead ECG offers valuable help in the early identificationof successful recanalization of infarct-related arteries afterthrombolytic therapy in patients with acute myocardial infarction.Use of the ratio of ST segment normalization according to theseparate criteria for anterior and inferiorllateral infarctsgives the test a high sensitivity and specificity, even in thepresence of interventricular conduction disturbances.     

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.     

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.     

Nitroglycerin and afterload: effects of aortic compliance and capacity of the Windkessel

The effect of nitroglycerin (NTG) is mainly a reduction in preloadand afterload. The decrease in afterload may be caused by afall of total systemic resistance (TSR) or by an increase ofarterial compliance (AC). The effects of NTG on TSR and AC weretested in 10 patients given 1.6 mg NTG sublingually. The capacityof the whole Windkessel (C) was calculated as C=/TSR ( = timeconstant of the diastolic aortic pressure decay). The diameterof the descending thoracic aorta was measured from an aortogram.Aortic stiffness SAO) was calculated SAO = P/D. Since mean aorticpressure decreased by 6% after NTG without any change in cardiacindex or heart rate, there had to be a primary reduction ofafterload as measured from mean systolic resistance (–9%).This reduction of afterload could not be related to a decreasein TSR and SAO, C, however increased by an average of 27%. These data indicate that NTG decreases the muscular tone ofpostaortic muscular vessels and, hence, increases the Windkesselcapacity, while aortic compliance does not change.     

A late increase in free radical activity post myocardial infarction

Free radicals (FR) are a highly reactive chemical species whichhave been implicated in the pathogenesis of reperfusion injury.Experimental models of reperfusion injury have demonstratedthat FR scavengers improve myocardial salvage and thus it hasbeen postulated that they may be of benefit in acute myocardialinfarct (MI) patients treated with thrombolysis. Previous studiesof FR activity post MI have focused on the immediate post reperfusionperiod; the present study investigates FR activity in post MIpatients over a longer time span. Free radicals have a very short half-life and in clinical studiestheir activity is usually assessed indirectly by measuring eitherthe level of FR reaction products such as malondialdehyde (MDA)or FR scavengers such as plasma thiols (PSH). In the presenceof increased FR activity MDA levels increase and PSH levelsdecrease. Twenty-two acute MI patients had blood samples taken on admission,day 7 and day 21 post MI for measurement of MDA and PSH levels.On day 7 post MI a significant increase in MDA was detectedP=0.0001 (Sign test) (median change +2.1 µmol. I) anda significant decrease was detected in PSH P = 0.04 (Sign test)(median change, – 38 µmol. l^–1). No significantdifferences were detected between admission and day 21 levelsof MDA and PSH. This study demonstrates the presence of enhanced FR activityat a later time point than has previously been recognised. Whiteblood cells utilise FRs during phagocytosis and the late risein FR activity detected in this study may reflect white bloodcell removal of necrotic myocardium.     

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.     

Increased neutrophil aggregability in coronary artery disease

The purpose of this investigation was to study neutrophil (PMN)aggregation in the aorta and coronary sinus of 20 patients withangiographically documented coronary artery disease (group I)compared with eight patients with normal coronary arteries (groupII). PMNs were separated from the other blood components andtheir aggregation response to Ca²⁺ ionophore A 23187 1 x 10^–5M (final concentration) was measured. Group I patients had higher aggregating activity in the coronarysinus than in the aorta (24.9± 3.7 vs 18.7± 3.4average maximum T, P<0.01), while no difference was foundin group II (coronary sinus 16.7±3.5; aorta 16.3±2.4average maximum TP = NS). Among group I patients, smokers hada significantly higher aggregating activity than non-smokers,whereas no correlation was found between aggregation responseand blood cholesterol values. These data suggest that the presence of atherosclerotic plaquesin coronary vessels may prime PMNs so that they show greateraggregating response to subsequent stimulation.     

OSTEOLYTIC PROPERTIES OF THE SYNOVIAL-LIKE TISSUE FROM ASEPTICALLY FAILED JOINT PROSTHESES

Relationships were found between the bone-resorbing abilityof conditioned media (CMs) from cultures of peri-prosthetictissues and their levels of bone-remodelling agents. Bone-resorbingactivity was measured by ⁴⁵Ca release from pre-labelled mousecalvaria and 23 of 40 CMs exhibited bone-resorbing activity.Cytokine and prostanoid levels in the CMs were measured by immunoassay,and the levels of interleukin (IL)-1ß, IL-6, tumournecrosis factor (TNF) and prostaglandin E₂ (PGE₂) correlatedwith each other, except for the latter two. Significantly higherlevels of IL-6 were present in those CMs with bone-resorbingactivity than in those without, and a similar pattern was observedfor PGE₂ and IL-1ß. However, some CMs with high levelsof IL-1ß, IL-6, TNF and PGE₂ failed to induce resorption,whereas a few CMs with low levels of these agents induced resorption.Moreover, neither dialysis of CMs nor addition of neutralizingantisera to IL-1 and IL-1ß to CMs, either alone orin combination, reduced the bone-resorbing activity of the CMs.It is considered that these agents may act synergistically tomediate osteolysis around failed joint implants, but that otherunidentified bone-resorbing agent(s) must be involved. KEY WORDS: Implant failure, Pseudosynovial membrane, IL-1ß, IL-6, TNF, TGFß1, Prostaglandins, Bone resorption, Leucocytes     

Reassessment of the relation between QRS forces of the orthogonal electrocardiogram and left ventricular ejection fraction

Previous studies have demonstrated the existence of a strongpositive correlation between the amplitude of QRS forces ofthe orthogonal electrocardiogram and the angiographically determinedleft ventricular ejection fraction. In a large group of patientsevaluated for chest pain, we examined the relationship betweenthe arithmetic summation of R_x+R_y+Q_z (R) the maximal and meanspatial QRS vectors and the ejection fraction (EF). In a totalof 252 patients, there was a statistically significant correlationbetween R and EF but a low correlation coefficient value (r:0.22, P<0.001). This relationship was essentially due tothe group of patients with coronary artery disease and myocardialinfarction (r: 0.24, P<0.015) whereas there was no correlationin the group of normal subjects or in patients with coronaryartery disease without myocardial infarction. In the group withmyocardial infarction, a significant correlation between R andEF existed only in patients with anterior myocardial infarction(r: 0.41, P<0.025). In conclusion, both ejection fractionand amplitude of QRS forces decrease in coronary artery diseaseespecially when an anterior myocardial infarction is present.However, despite the positive association between these angiographicand electrocardiographic indices, the low value of the correlationcoefficient indicates that it is not possible to predict ejectionfraction from the value of R in individual patients.     

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.     

SULPHASALAZINE THERAPY IN ANKYLOSING SPONDYLITIS: ITS EFFECT ON DISEASE ACTIVITY, IMMUNOGLOBULIN A AND THE COMPLEX IMMUNOGLOBULIN A-ALPHA-1-ANTITRYPSIN

Serum levels of immunoglobulin A (IgA) and the complex immunoglobulinA-, antitrypsin (IgA-¹ AT) were measured at the commencementand after 3 months of a double-blind, placebo-controlled trialof sulphasalazine (SAS) in patients with active ankylosing spondylitis(AS). Twenty-eight patients were evaluated, 15 on sulphasalazine,13 on placebo. Significant falls were seen in both IgA (p<0.01)and IgA-₁AT (p<0.001) in the actively treated patients. Inaddition, significant improvement in clinical and laboratorymeasures of disease were observed. It is concluded that SASis effective in AS and modulates the immune response. KEY WORDS: Sulphasalazine, Ankylosing spondylitis, Immunoglobulin A, Immunoglobulin A-₁anti-trypsin complex, Controlled trial     

LACK OF CORRELATION BETWEEN CLINICAL DISEASE ACTIVITY AND ERYTHROCYTE SEDIMENTATION RATE, ACUTE PHASE PROTEINS OR PROTEASE INHIBITORS IN ANKYLOSING SPONDYLITIS

Disease activity was assessed clinically and erythrocyte sedimentationrate (ESR), C-reactive protein (CRP), orosomucoid, ₁-antitrypsin(₁ AT) and ₂-macroglobulin (₂M) were measured in 65 patientswith ankylosing spondylitis (AS). Positive correlations werefound between ESR and the acute phase proteins (APP), CRP, orosomucoidand ₁AT, but none of these variables correlated with the clinicalassessment of activity. No relationship was demonstrated betweenthe protease inhibitor, ₂M and clinical activity, ESR or anyof the APP. While the treatment of AS remains predominantly symptomatic,routine management of patients should continue to be foundedon the clinical assessment of disease activity rather than onlaboratory indices of inflammation. KEY WORDS: Ankylosing spondylitis, Clinical assessment, Erythrocyte sedimentation rate, Acute phase proteins, Protease inhibitors     

Influence of aortic regurgitation on the assessment of the pressure half-time and derived mitral-valve area in patients with mitral stenosis

The influence of aortic regurgitation on the Doppler assessmentof pressure half-time (T) and on the derived calculation ofthe mitral-valve area has not yet been adequately evaluatedin patients with mitral stenosis and associated aortic regurgitation.Therefore this study was undertaken to verify the accuracy ofthe T method for the noninvasive estimation of mitral-valvearea in patients with mitral stenosis and associated aorticregurgitation. Data were obtained from 31 selected patientswho underwent cardiac catheterization within 24 h of the noninvasiveexamination. From the Doppler velocity curve, T was calculatedas the interval between the peak transmitral velocity and velocity/. Mitral-valve area was measured fromthe T with a computerized system using the equation: 220/T,in cm². Calculation of the mitral-valve area at catheterizationwas derived applying the modified Gorlin formula. Mean mitral-valvearea, as determined at catheterization, ranged from 0.5 to 2.8cm² (1.3±0.6). Mean mitral-valve area, as calculatedby continuous-wave Doppler, ranged from 0.7 to 2.7 cm² (1.5± 0.6). Linear-regression analysis of data revealed agood correlation between Gorlin and Doppler measurements ofthe mitral-valve area (r = 0.90, SEE = 0.28 cm², P<0.001,y = 1.0x + 0.2). Doppler showed a systematic overestimate ofthe mitral-valve area (26%) in patients with mitral stenosisand aortic regurgitation as compared to the Gorlin formula.The overestimate of continuous-wave Doppler was even greater(39%) in a subgroup of patients with 2 + or 3 + angiographicaortic regurgitation. Thus the Doppler T method still providesaccurate noninvasive estimates of mitral-valve area in patientswith mitral stenosis and associated aortic regurgitation. However,when the degree of aortic regurgitation is significant, Dopplercan lead to important overestimation of the mitral orifice size.