Enhanced sensitivity for detection of coronary artery disease by addition of atropine to dipyridamole echocardiography

Dipyridamole echocardiography test (DET) has gained acceptancedue to its safety, feasibility, diagnostic accuracy and prognosticpower. The main limitation of the test is a less than idealsensitivity in some patient subsets, such as those with limitedcoronary artery disease. Atropine with dipyridamole might theoreticallycombine to become a synergistic ischaemic stress test, by increasingmyocardial oxygen demand through chronotropic stress and byreducing flow supply through a shortening of the diastolic intervalunder maximal coronary vasodilation. The aim of this study wasto assess the effects of the addition of atropine to DET. Threehundred and twenty-one patients (age=58±9 years), referredfor testing in the echo lab, were initially studied by DET.Of these, 151 were stopped during or within the 2 min followingdipyridamole infusion because of achievement of a predeterminedend-point: obvious echocardiographic positivity (n = 137), severechest pain (n = 3), diagnostic ST segment changes (n = 7) orlimited side effects (n = 4). In another three cases, atropinewas not given due to a history of glaucoma or severe prostatichypertrophy. In the remaining 167 patients with a negative DETtest, atropine (0.25 mg intravenously, repeated every min upto a maximum of 1 mg, if necessary) was added, starting 3 minafter the end of the dipyridamole infusion. The dipyridamole-atropineecho test (DETA) was positive in 32 and negative in 135 patients,and no major side effects occurred in any patient. The peakheart rate was significantly higher during DETA than with DETalone (108±16 vs 86±14 beats . min^–1; P<0.0001).In the subset of 178 patients who were studied while not takingantianginal therapy, who had no prior myocardial infarctionor revascularization procedure and who underwent coronary catheterization,independently of the test results, coronary angiography showednormal coronary arteries in 48 patients and significant coronaryartery disease (CAD) ( 50% luminal reduction in at least onemajor coronary vessel by quantitative coronary arteriography)in 130 patients—with single-, double- and triple-vesseldisease in 56, 47 and 27 patients, respectively. The sensitivitywas 96/130 for DET and 110/130 for DETA (72 vs 85%, P<0.01)while the specflcity was 96% and 92% (P=ns), respectively. Theaddition of atropine to dipyridamole, which causes further chronotropicstress to the myocardium already challenged by flow maldistribution,is well tolerated and safe, and increases the sensitivity ofthe test for the detection of coronary artery disease with noloss in specificity.     

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression

The significance of anterior ST segment depression in inferioracute myocardial infarction (AMI) remains controversial. Theaim of this study was to relate precordial ST segment depressionto the topography of residual myocardial ischaemia, with myocardialmapping of the asynergic area and coronary anatomy. Twenty-fivepatients with first inferior AMI (15 patients with anteriorST segment depression: group A and 10 patients without anteriorST segment shift: group B), all underwent: (1) electrocardiographicevaluation on admission to the Coronary Care Unit and at 24h intervals thereafter; (2) 2D-echocardiographic study within3 h of CCU admission: (3) dipyridamole echocardiographic test(DET) (doses of dipyridamole up to 0.84 mg.kg^–1 i.v. over10 min) 4 days after AMI; (4) coronary arteriography within14 days from AMI. To assess regional left ventricular wall motion,a 16 segment model was used and a wall motion score index (WMSI)was derived. The results of DET were correlated to the anatomyof the infarct-related vessel. Compared to group B, group Apatients showed a significantly greater maximal ST segment elevationin inferior limb leads (lead III: 3.9±1.9 mm vs 2.2±1.1mm, P<0.05; aVF: 3.5±13 mm vs 1.7±0.8 mm, P<0.001).Group A patients showed greater WMSI (1.35±0.22 vs 117±0.12,P<0.05), with more frequent postero-lateral wall involvement(72% vs 20%, P<0.05). No patient of either group showed asynergyof the anterior, anterolateral or anteroseptal segments. Nodifferences in the distribution of coronary artery disease wereobserved. Left anterior descending coronary artery disease waspresent in only three patients (20%) in group A and in one patientin group B. DET was positive in eight patients (53%) in groupA and in three (30%) in group B (P = statistically not significant).In all patients DET induced new wall motion abnormalities locatedin the territory of the infarct-related artery. None of thepatients developed new wall motion abnormalities remote fromthe infarct zone or adjacent to the infarct zone, but locatedin different vascular regions. In conclusion, anterior ST segmentdepression in inferior A MI appears to indicate a more extensivearea of asynergy, with frequent involvement of the posterolateralwall. The topography of DET-induced residual myocardial ischaemiadoes not support the hypothesis of concomitant anterior ischaemia.     

Prognostic value of echocardiography with high-dose dipyridamole after recent uncomplicated myocardial infarction

The feasibility, safety and prognostic importance of high-dose (0.84 mg/kg over 10 minutes) dipyridamole 2D echocardiography test (DET) were evaluated in 78 asymptomatic patients 10 to 14 days after uncomplicated acute myocardial infarction and the results were compared with those of exercise stress test (EST). Criteria of positivity were: for DET a new or worsening asynergy; for EST, ST segment depression greater than or equal to 1 mm (patients were in complete pharmacological wash-out). Patients were followed-up for 9 to 22 months (mean 14 +/- 5) or until one of the following end-points occurred: death, infarction or severe angina. DET was positive in 13/17 patients and EST in 5/17 patients with poor clinical outcome (sensitivity 76% vs 29%; p less than 0.005); for hard events only (death or infarction) sensitivity was respectively 64% vs 9%; (p less than 0.05). Both tests had the same specificity (92%). Cumulative event-free survival curves as a function of DET and EST results were both statistically different (p less than 0.001 and p less than 0.05 respectively). Cumulative survival curves obtained by the combination of DET and EST results showed: 1) an uneventful course in patients with both tests or only DET negative; 2) and a poor clinical outcome in patients with both test or only DET positive (p less than 0.001) DET correctly predicted clinical outcome in 12/16 patients in whom there was disagreement between the two tests. We conclude that DET is more sensitive than EST for identifying patients at increased risk for coronary events and more accurate for predicting clinical outcome after uncomplicated acute myocardial infarction.     

Dipyridamole echocardiographic test performed 3 days after an acute myocardial infarction: feasibility, tolerability, safety and in-hospital prognostic value

In recent years, increasing evidence has pointed to the potentialof dipyridamole stress echocardiography as a fast, effective,inexpensive method of risk stratification after an acute myocardialinfarction. A very early stratification by this test could improvethe patient's management and reduce the duration of in-hospitalstay, and, thus, the costs. Two-hundred and fifty-one consecutive patients (208 male, age58 ± 11) with a two-dimensional echocardiogram of goodtechnical quality underwent a dipyridamole echocardiographictest (DET) 70 ±6 h after an acute myocardial infarction.Criterion for positivity was the identification of a transientregional asynergy that was absent or of a lower degree in thebaseline examination. Positivity was defined as ‘at low-dose’or ‘at high- dose’ if the asynergy was detectedbefore or after the 8th min of a drug infusion. All tests wereperformed without any major side effects. DET was positive in149 (59%) and negative in 102 (41%) patients. During the hospitalstay, cardiac events (death, reinfarction, angina) occurredin 521251 patients: in 491149 with a positive and in 31102 witha negative test (sensitivity 94%, negative predictive value97%, P<000001). Severe events (death and reinfarction) occurredin 14/251: in 121149 with a positive DET and in 21102 with anegative DET (sensitivity 86%; negative predictive value: 98%;V<0.05). Moreover, cardiac events occurred in 28165 patientswith a low-dose positive DET, in 21184 with a high-dose positiveDET and in 31102 with a negative DET (low-dose positive vs negativeDET: P<0 00001, and vs high-dose positive DET: P<002;high-dose positive vs negative DET: P<000001). Hence, DETperformed 3 days after acute myocardial infarction is feasible,well tolerated and safe, and allows early stratification ofpatients with different degrees of risk of in-hospital cardiacevents.     

High-dose dipyridamole echocardiography test in coronary artery disease after heart transplantation

In order to evaluate the usefulness of high-dose dipyridamoleechocardiography test (DET) for the detection of coronary arterydisease (CAD) after heart transplant and for the assessmentof prognosis, 80 heart transplant patients underwent this testwithin 48 h of tile scheduled yearly coronary angiography. Coronary angiography showed normal coronary arteries in 55 patientsand CAD in 25, eight of whom had >50% luminal narrowing.Segmental hypokinesis on baseline echocardiography was presentin 27 patients, 19 of whom had CAD (sensitivity = 76%; specificity= 85%). DET was negative in all the patients with normal coronaryarteries (specificity 100%). Out of 25 patients with CAD, eighthad a positive DET and 17 a negative DET (sensitivity 32%),but DET was positive in seven of the eight patients with coronaryartery stenosis >50% (sensitivity 87%). During follow-up(9.8±4.5 months) seven cardiac events occurred in sevenpatients, all with CAD and wall motion hypokinesis (six on baselineechocardiogram and four after dipyridamole infusion). In our experience, DET does not seem adequate for the screeningof post-transplant CAD, but useful in identifying patients withsevere lesions (>50%). Wall motion abnormalities on baselineechocardiogram or after dipyridamole infusion might identifypatients who require closer surveillance. A longer experienceis needed to confirm these results.     

Detection of significant residual stenosis of the infarct-related artery after thrombolysis by high-dose dipyridamole echocardiography test: Is it detected often enough?

Background and hypothesis: It has been reported that high-dose dipyridamole echocardiography test (DET) can be successfully used for the detection of critical residual stenosis of the infarct-related artery (IRA). However, we have recently noticed low sensitivity of DET for the detection of residual IRA stenosis in patients with single-vessel disease. This study sought to determine the value of DET for the detection of significant residual stenosis of the IRA after thrombolysis. Methods: Dipyridamole echocardiography test was performed in 55 consecutive patients after a first acute myocardial infarction before hospital discharge. All patients underwent coronary angiography 23 ± 6 days after infarction. Results: Nine of 19 patients with positive DET revealed new adjacent asynergy and all of the patients had patent and significantly stenotic IRA. Sensitivity and specificity of DET in identifying significant residual stenosis of the IRA were 24 and 100%, respectively. Among 49 patients with significantly stenotic or occluded IRA, 40 patients without adjacent asynergy during DET had higher baseline wall motion score index (WMSI) compared with 9 patients who revealed adjacent asynergy during DET (1.45 ± 0.30 vs. 1.24 ± 0.18; p<0.05). When all patients with positive DET (adjacent or remote asynergy) were compared with those with negative DET, no difference in baseline WMSI was found (1.37 ± 0.24 vs. 1.44 ±0.24;p>0.05). Conclusions: Our data indicate that sensitivity of DET in detecting significant residual stenosis of the IRA after thrombolysis is low. It seems that the extent of myocardial infarction affects the ability of DET to detect adjacent, but not remote asynergy.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3·5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4·7 ± 0·5 vs 4·6± 0·6 for the left anterior descending, 4·6± 0·4 vs 4·6 ± 0·3 for theleft circumflex and 4· ± 0·4 vs 4·4± 0·5 for the right coronary artery (all P=non-significant).The subsets of mitral valve prolapse patients with differentclinical ‘ischaemic’ manifestations were similarin terms of the calculated coronary flow reserve in all threemajor epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Role of blood pressure response to provocative tests in the prediction of hypertension inadolescents

To assess the value of exercise stress testing and of mentalstress as predictors of hypertension, we studied 130 normotensivemales 14–18 years of age. Sixty-five had at least onehypertensive parent (SHT), while 65 had normotensive parents(SNT). Systolic (SBP) and diastolic (DBP) blood pressure, rate-pressureproduct (RPP) and 12-lead ECG were recorded at rest, throughoutthe tests and during the recovery phase.The two groups werenot significantly different at rest for the examined variables.However, the SHT group showed a greater average SBP than theSNT group (198.4±18.7 vs 189.5±14.9 mmHg; P<0.05)at the peak of exercise. A significantly higher proportion ofSHT subjects (40.0% vs 18.5%: P<0.01) had SBP >200 mmHg.No difference in the ECG pattern between the two groups wasobserved.During mental stress, no significant differences inthe examined variables between the two groups were noted, althoughSBP, DBP, HR and RPP were slightly higher in SHT than in SNTsubjects.These data suggest that the SBP response to dynamicexercise may be a good predictor of hypertension in subjectsat risk.     

Dipyridamole-echocardiography test in angina at rest: noninvasive assessment of coronary stenosis underlying spasm

In a previous study performed in patients with effort angina pectoris, we showed that the dipyridamole-echocardiography test (DET) is feasible and useful for the detection of coronary artery disease. The positivity of the test (consisting of two-dimensional echocardiography [2 DE] combined with dipyridamole infusion [0.14 mg/kg/min for 4 minutes]) is linked to the appearance of regional asynergy. In the present study, DET and exercise stress test (EST) were performed in 62 patients with angina at rest in the active phase. The overall sensitivity of DET and EST for the detection of coronary artery disease was 62% and 83%, respectively (p less than 0.05); the specificity of DET and EST was 100% and 64%, respectively (p less than 0.05). In 10 DET-positive patients, a spontaneous attack was also monitored by 2DE; the myocardial wall involved by ischemia was invariably the same both in patients with spontaneous and in those with dipyridamole-induced ischemia. Thus, in our population of patients with angina at rest (in whom an important functional component is also likely to be present during exercise), DET was significantly less sensitive but significantly more specific than EST in detecting coronary artery disease.     

Relationship between ventilatory threshold and onset of ischaemia in ECG during stress testing

The study was carried out to determine the relationship betweenventilatory threshold and the onset of ischaemia, as shown onthe ECG (horizontal and/or descending ST depression of 0.05mV, on average). Twenty-seven male patients (aged 58 ±7 years) with angiographically documented coronary artery disease(CAD) were assessed by cardiopul-monary exercise testing withoutmedication. Oxygen uptake (VO₂), heart rate (HR), rate-pressure-product(RPP) and blood lactate were measured and/or calculated every30 s during exercise. In addition, 10 patients, comparable withthe above group, were examined to find out the acute effectsof isosorbide dinitrate (ISDN) at ventilatory threshold in relationto ischaemic threshold. The first cardiopulmonary exercise testwas carried out without medication, the second 1 h later with5 mg ISDN, taken sublingually 30 min before the test. RESULTS: (x SD): (1) The mean ventilatory threshold preceded the ischaemicthreshold in relation to exercise capacity (48 ±14 vs55±20 watts; P<0.05), VO₂. kg^–1 (10.0 ±2.2vs 12.0 ±2.9 ml. kg^–1. min; P<0.05), HR (93± 15 vs 100 ± 16. min ^–1; P<0.01), RPP(15095 ± 4424 vs 17166 ± 5245; P<0.01) andblood lactate (1.28 ± 0.53 vs 1.44 ±0.60 mmol.l^–1; P<0.05). (2) This relationship was observed moreoften in the subgroup of patients with angina during cardiopulmonaryexercise testing or with myocardial infarction or with three-vesseldisease than in patients without angina or infarction or withone- and two-vessel disease. (3) ISDN improved the ischaemicthreshold from 55 ±26 watts (without medication) to 81±32 watts (P<0.01) but not the ventilatory threshold(56 ±23 vs 59 ±21 watts, ns). CONCLUSION: The ventilatory threshold seems to precede the ischaemic thresholdbecause of impaired aerobic capacity of the leg muscles, causedby deconditioning on account of the disease. However, ischaemia-inducedleft ventricular dysfunction did not seem to have a direct influenceon ventilatory threshold as ISDN improved the ischaemic threshold,but not the ventilatory threshold.     

Early ventricular fibrillation in patients with acute myocardial infarction: correlation with coronary angiographic findings

To define coronary angiographic characteristics of patientsexperiencing early primary ventricular fibrillation (VF) inthe acute phase of myocardial infarction we studied 266 consecutivepatients without clinical evidence of heart failure. Twenty-sixpatients (group 1) experienced early (< 12 h from the onsetof symptoms of myocardial infarction) primary VF whereas 240patients (group 2) with the same clinical characteristics servedas an appropriately matched cohort. All patients were catheterizedbefore or soon after hospital discharge (1 to 8 weeks afterthe acute event). There was no significant difference in left ventricular ejectionfraction between the two groups of patients (39.6±6%vs 36.9±8%, P = ns). Patients with early VF had a significantlygreater number of diseased vessels than those without VF (3.38±1.05vs 2.03±1.25. P <0.001) and a higher coronary arteriographicGensini score (29.31±4.80 vs 20.16±4.14, P <0.001).The left anterior descending coronary artery was identifiedas the infarct-related vessel in 53.6% of group 1 vs 44.5% ofgroup 2 patients (P <0.05). The mean maximal serum creatinekinase values were not significantly different (1897±1062vs 1426 ±839 IU.l–1, P=ns) between the two groups. These data indicate that patients with early primary VF in thesetting of acute myocardial infarction may have more extensivecoronary artery disease than similar patients without VF. Aworse prognosis could be anticipated for these patients on thebasis of worse coronary anatomy. A more aggressive therapeuticapproach with routine coronary angiography before hospital dischargecould reasonably be justified for patients with early primaryVF complicating acute myocardial infarction.     

Gold 195m in the assessment of the cold pressor test by first pass radionuclide ventriculography

First pass radionuclide ventriculography was performed withgold 195m in a sequential evaluation of left ventricular ejectionfraction during cold pressor stimulation. We studied 10 normalcontrols, 10 patients with angina pectoris who had proven coronaryartery disease and normal left ventricular function during contrastangiography and 10 patients with dilated cardiomyopathy withnormal coronary arteries and impaired left ventricular functionat contrast angiography. Mean resting ejection fraction was similar in controls and patientswith coronary heart disease (57 ± 2 vs 58 ± 3)but was significantly lower in the cardiomyopathic subjects(27 ± 4, P < 0.001). After 30 seconds cold pressorstimulation, mean left ventricular ejection fraction fell inthe normal controls (57 ± 2 to 52 ± 2, P <0.05)but was unchanged in those with coronary heart disease and dilatedcardiomyopathy (58 ± 3 to 55 ± 3 and 27 ±4 to 24 ± 4, both NS). No further significant changeoccurred after 2.5 minutes stimulation (53 ± 1, 58 ±3 and 23 ± 3, respectively). There was no differencein the pattern of left ventricular ejection fraction responsebetween the groups. Six controls, 4 patients with coronary heartdisease and 4 patients with dilated cardiomyopathy had a significantfall in left ventricular ejection fraction and 4, 5 and 6, respectively,developed a new or further deterioration in regional wall motion.Thus neither changes in regional wall motion nor left ventricularejection fraction response distinguished either patient groupfrom the normal controls. We do not recommend cold pressor stimulationas a diagnostic test for coronary heart disease.     

Normal coronary flow reserve in patients with mitral valve prolapse, a positive exercise test and normal coronary arteries

We studied 12 patients (eight females and four males), ages30–46 years, with echocardiographically documented mitralvalve prolapse and clinical suspicion of coronary artery disease,based on a history of chest pain (five patients), angina-likepain (three patients), a positive exercise stress electrocardiogram(12 patients) and a focally positive thallium-201 stress perfusionscan (three patients), who were referred for cardiac catheterizationand found to have normal coronary arteries. Ten patients withoutevidence of heart disease served as controls. In all mitralvalve prolapse patients, coronary flow velocity reserve wasdetermined successively in the left anterior descending, leftcircumflex and right coronary arteries as the ratio of the maximun(after intracoronary papaverine) to the resting mean coronaryflow velocity. Coronary flow reserve values were fairly similarin the mitral valve prolapse and control patients; all 12 mitralvalve prolapse patients had normal coronary flow reserve (3.5)in all three coronary arteries with no significant differencesamong the arteries tested Mean values ± 1 standard deviationof the coronary flow reserve (mitral valve prolapse vs controlpatients) were 4.7 ± 0.5 vs 4.6 ± 0.6 for theleft anterior descending, 4.6 ± 0.4 vs 4.6 ± 0.3for the left circumflex and 4. ± 0.4 vs 4.4 ±0.5 for the right coronary artery (all P=non-significant). Thesubsets of mitral valve prolapse patients with different clinical‘ischaemic’ manifestations were similar in termsof the calculated coronary flow reserve in all three major epicardialcoronary arteries. In conclusion, this study demonstrated that an inadequate regionalcoronary flow reserve does not account for the clinical manifestationsof myocardial ischaemia and positive exercise tests in patientswith mitral valve prolapse and normal coronary arteries.     

Gradient-echo magnetic resonance imaging during incremental dobutamine infusion for the localization of coronary artery stenoses

Dobutamine pharmacological stress testing in conjunction withgradient-echo magnetic resonance imaging (MRI) may be a usefultool for the assessment of haemodynamically significant coronaryartery stenoses. Therefore, 28 patients without previous myocardialinfarction but significant proximal stenoses (70% diameter stenosis)of one or more coronary arteries were selected for dobutamine-MRI.Each patient underwent MRJ at rest and during incremental dobutamineinfusion (5, 10, 15 and 20 µg. kg^–1. min^–1).Additionally, all patients were submitted to exercise stresselectrocardiography (EST). A total of 72 segments per patient obtained from identical shortaxis and transverse tomograms at rest and during dobutamineinfusion were evaluated by two observers. Each segment was gradedas normal, hypokinetic, akinetic or dyskinetic. Dobutamine-MRIwas considered pathological if segmental wall motion deterioratedby at least one grade after dobutamine infusion. For comparisonwith coronary angiography, segmental wall motion gradings wererelated to the respective coronary artery territories. Peakrate-pressure product during steady-state dobutamine infusion(18·493 ± 4·315 mmHg. min^–1) wassignificantly lower (P<0·01) than during EST (21·316± 4·937 mmHg. min^–1). Dobutanine-inducedwall motion abnormalities were observed in 22/26 (85%) MR studiesand 20/26 (77%) patients had a pathological EST. Regional asynergyinduced by dobutamine-MRI occurred in 11/15 (73%) patients withsingle and 11/11 (100%) with multi-vessel disease. Sensitivityand specificity for the detection of a stenosed coronary arterywere 87% and 100% for the left anterior descending, 62% and93% for the left circumflex and 78% and 88% for the right coronaryartery respectively. In conclusion, dobutamine-MRI is a well tolerated, non-exercisedependent test for the detection and localization of hzaemodynamicallysignificant coronary artery stenoses with a diagnostic accuracysimilar to that previously reported for high-dose dipyridamoleMRI but with a better control of stress intensity and duration.     

Comparison of the high-dose dipyridamole-echocardiography test and exercise two-dimensional echocardiography for diagnosis of coronary artery disease

Fifty-five patients with effort angina pectoris and technically satisfactory baseline echocardiograms performed a supine exercise-echocardiography test (EET) and a high-dose dipyridamole-echocardiography test (DET, up to 0.84 mg/kg of intravenous dipyridamole in 10 minutes). All underwent coronary arteriography, which showed that at least 1 major artery had more than 70% stenosis in 34 patients. For each patient, the same physician performed both tests, with the same echocardiographic equipment. Detection of new onset or worsening regional asynergy was the only criterion of positivity for both tests. DET yielded interpretable studies in all 55 patients (100%); EET yielded only 40 such studies (73%) (p less than 0.01). In the 40 patients in whom both tests were interpretable, DET showed, compared with EET, a similar sensitivity (72% vs 76%) and specificity (100% vs 87%) (difference not significant for both) for detecting angiographically assessed coronary artery disease. In the 16 patients in whom both DET and EET yielded positive responses for ischemia, the same myocardial region showed reversible asynergy. Thus, independent of all factors that can affect the performance of each test (operator, patient and instrumentation), DET was significantly more feasible than EET, with comparable sensitivity and specificity. Dipyridamole provokes asynergy in the same regions that show ischemia during exercise.     

Value of exercise radionuclide ventriculography and thallium-201 scintigraphy in evaluating successful coronary angioplasty: comparison with coronary flow reserve, translesional gradient and percent diameter stenosis

Assessment of percutaneous transluminal coronary angioplasty(PTCA) by early radionuclide exercise test was evaluated for11 arteries undergoing a successful procedure. Exercise thallium-201(Tl-201) and radio-nuclide ventriculography (RNV) were performedwithin 3 days before and after PTCA and compared to % diameterstenosis, % translesional gradient and regional coronary flowreserve (CFR) determined by digital coronary angiography. Primarysuccess of the procedure was gauged by reduction in % stenosisfrom 80 ± 12% to 31 ± 12% (residual stenosis <50% in all cases) and reduction in % gradient < 25% in allcases). Before PTCA, Tl-201 and/or RNV were abnormal in allcases. After PTCA, radionuclide exercise tests improved butremained abnormal in 4 instances. No relationship was foundbetween residual % gradient or stenosis and pathological Tl-201or RNV following PTCA, but abnormal tests were observed among4 out of the 5 vessels with the lowest CFR ( < 1.69). Inone case CFR remained depressed despite good angiographic, hemodynamicand scintigraphic results, this patient had unstable anginabefore the procedure. Among patients with stable symptoms, CFRof arterial distributions with positive Tl-201 or RNV afterPTCA was significantly lower than that with negative tests (1.58± 0.05 as compared to 1.90±0.25, P<0.02). Earlyradionuclide stress tests results thus reflect the physiologicimprovement of coronary circulation. They may reflect the persistenceof coronary flow abnormalities despite the relief of the epicardialstenosis.     

Argument for a Doppler echocardiography during exercise in assessing asymptomatic patients with severe aortic stenosis

Aims: Exercise stress testing (EST) is recommended by guidelines torisk-stratify patients with asymptomatic valvular aortic stenosis(AS), though the role of quantitative exercise-Doppler echocardiographyhas rarely been studied. This prospective study sought to correlatestandard EST results with the haemodynamic measurements madeduring exercise by Doppler echocardiography. Methods and results: We performed rest and semi-supine exercise Doppler echocardiographyin 44 consecutive patients (mean age = 68 ± 12 years)with aortic valve areas 0.6 cm²/m². The effective aortic valvearea (EOA), cardiac output (CO), maximal transvalvular velocity,and pulmonary pressure were monitored over the test. No seriousadverse event was observed. EST was positive in 26 (Group 1)and negative in 18 (Group 2) patients. Baseline echocardiographicmeasurements were similar (EOA 0.77 ± 0.15 vs. 0.78 ±0.14 cm²; CO 5.5 ± 1.6 vs. 5.9 ± 2 L/min) in bothgroups. Exercise-induced changes in CO (+2.9 ± 2 vs.+4.3 ± 1.8 L/min, P = 0.04) and EOA (–0.04 ±0.18 vs. +0.15 ± 0.24 cm², P = 0.015) were significantlygreater in Group 2. A correlation between changes in EOA andchanges in CO during exercise was observed, but significantlyhigher in Group 2 (P = 0.04). Conclusion: In the presence of severe asymptomatic AS, exercise Dopplerechocardiography, assessing the mechanisms behind a positiveEST, appears very promising but further studies with prognosisassessment remain necessary.     

Angioscopic evaluation of prolonged vs standard balloon inflations during coronary angioplasty: A randomized study

To study the immediate effects of prolonged total balloon inflationduring PTCA, 41 patients (44 lesions) with chronic-stable anginawere randomized for prolonged sequential inflations (three tofive inflations of 3 to 5 min each, for a total duration of 12 min, group 1, n=20 lesions) or ‘standard’ sequentialinflations (three to five inflations of 1 min each, for a totalduration of 3 min, group 2, n-24 lesions). The mean durationof total balloon inflation time was 958 ± 129 s in group1 vs 205 ±46 s in group 2. Results of angioplasty wereassessed on both angiography and percutaneous transluminal coronaryangioscopy performed immediately after the procedure. High qualityimaging of the coronary lumen and lesion morphology was possibleon angioscopy in all patients without any complications. Post-PTCAangiographic percent diameter stenosis was significantly lessin group 1 compared to group 2: 26 ± 10% vs 36 ±8% (P<0.05). On angioscopy, flaps were seen in 16 patientsin group 2, but in only six in group 1 (P<0.02). There wasno difference in the incidence of thrombi on angioscopy betweenthe two groups (group 1: nine cases, group 2: 10 cases). Sensitivityof angiographic detection of flaps and thrombi was poor: 10%and 12% respectively. One patient in each group developed alongitudinal dissection, detected on both angiography and angioscopy. Conclusions: (1) prolonged sequential balloon inflations leadto less residual luminal stenosis after PTCA, with a decreasedincidence of intimal flaps in comparison with standard inflations.(2) Post-PTCA transluminal coronary angioscopy is safe and offersbetter assessment of luminal effects of PTCA than angiography.     

Coronary microvascular dysfunction after elective percutaneous coronary intervention: Correlation with exercise stress test results

Objectives

We assessed whether exercise stress test (EST) results are related to the presence of coronary microvascular dysfunction (CMVD) in patients undergoing elective percutaneous coronary intervention (PCI).

Background

Previous studies showed that EST is poorly reliable in predicting restenosis after PCI; some studies also showed CMVD in the territory of the treated vessel.

Methods

We studied 29 patients (age 64 ± 6, 23 M) with stable coronary artery disease and isolated stenosis (> 75%) of the left anterior descending (LAD) coronary artery, undergoing successful PCI with stent implantation. EST and assessment of coronary microvascular function were performed 24 h, 3 months and 6 months after PCI. Coronary blood flow (CBF) response to adenosine and to cold-pressor test (CPT) was assessed in the LAD coronary artery by transthoracic Doppler echocardiography.

Results

Patients with ST-segment depression ≥ 1 mm at EST performed 24 h after PCI (n = 11, 38%) showed a lower CBF response to adenosine compared to those with negative EST (1.65 ± 0.4 vs. 2.11 ± 0.4, respectively, p = 0.003), whereas the difference in CBF response to CPT was not significant (1.44 ± 0.4 vs. 1.64 ± 0.3, respectively; p = 0.11). At 3-month and 6-month follow-up a positive EST was found in 12 (41%) and 13 (44%) patients, respectively; patients with positive EST also had lower CBF response to adenosine compared to those with negative EST (3 months: 1.69 ± 0.3 vs. 2.20 ± 0.3, respectively; 6 months: 1.66 ± 0.2 vs. 2.32 ± 0.3, respectively; p < 0.001 for both).

Conclusions

Positive EST after elective successful PCI consistently reflects impairment of hyperemic CBF due to CMVD, which persists over a follow-up period of 6 months.     

Both endothelium-dependent and endothelium-independent function is impaired in patients with angina pectoris and normal coronary angiograms

Background The aim of this study was to investigate both endothelium-dependentand endothelium-independent vasodilatation in syndrome X patients.Recently selective impairment of endothelium-dependent functionhas been reported in a small number of syndrome X patients.However, other investigators have reported impaired endothelium-independentfunction. Methods We infused the endothelium-independent vasodilatorspapaverine and glyceryl trinitrate, and endothelium-dependentvasodilator acetyicholine in the left coronary artery of 35patients with syndrome X and in 17 control subjects (atypicalchest pain, negative exercise test, and normal coronary angiograms).Coronary blood flow was measured with an intracoronary Dopplercatheter positioned in the proximal left anterior descendingcoronary artery, and the artery diameter was assessed usingquantitative coronary angiography. Result The mean increase in coronary blood flow in responseto a 12 mg dose of papaverine was significantly less in thesyndrome X group (185±74% vs 411 ± 59%, P0·001).The increase in coronary blood flow in response to acetylcholine,at doses of 1, 3, 10, and 30 µg. min^–1, was alsosignificantly lower in the syndrome X group (12±13 (P>0·05),41 ± 33, 57 ± 68, and 124 ± 87% (P>0·001))as compared to the control group (76 ± 49, 214 ±116, 355 ± 115, and 361 ± 74%). Conclusion These findings demonstrate that both endothelium-dependentand endothelium-independent dilatation of the coronary microvasculatureis impaired in syndrome X.