Dipyridamole-dobutamine echocardiography: a novel test for the detection of milder forms of coronary artery disease.

OBJECTIVES: This study was designed to assess the clinical, hemodynamic and diagnostic effects of the addition of dobutamine to dipyridamole echocardiography. BACKGROUND: Pharmacologic stress echocardiography with either dipyridamole or dobutamine has gained acceptance because of its safety, feasibility, diagnostic accuracy and prognostic power. The main limitation of the two tests is a less than ideal sensitivity in some patient subsets, such as those with limited coronary artery disease. We hypothesized that two pharmacologic stresses might act synergistically in the induction of ischemia by combining the mechanisms of inappropriate coronary vasodilation (with dipyridamole) and an increase in myocardial oxygen consumption (with dobutamine). METHODS: One hundred fifty patients (mean [+/- SD] age 51 +/- 11 years) referred for stress echocardiography were initially studied by dipyridamole-dobutamine echocardiography. The test was stopped during the dipyridamole step in 95 patients for achievement of a predetermined end point (obvious dyssynergy induced by lower or higher dipyridamole dose), and dipyridamole-dobutamine tests were performed in 55 patients (negative dipyridamole echocardiographic test). In the same 150 patients the dobutamine echocardiographic test (up to 40 micrograms/kg body weight per min) was performed on a separate day. RESULTS: Significant coronary artery disease (> 50% diameter stenosis of at least one major coronary vessel by quantitative coronary arteriography) was present in 131 patients (one vessel in 115; two vessels in 10, three vessels in 6), with normal coronary arteriography in 19. The feasibility of the dipyridamole-dobutamine test was 96%. Self-limiting side effects occurred in 5% of patients. The peak rate-pressure product was lowest during the dipyridamole test (132 +/- 30) and was comparable during the dobutamine (186 +/- 59) and dipyridamole-dobutamine tests (179 +/- 45, p = NS vs. dobutamine; p < 0.01 vs. dipyridamole). Sensitivity was 71% for dipyridamole, 75% for dobutamine and 92% for dipyridamole-dobutamine echocardiography (dipyridamole vs. dipyridamole-dobutamine, p < 0.01; dobutamine vs. dipyridamole-dobutamine, p < 0.01; dipyridamole vs. dobutamine, p = NS), whereas specificity was 89% for dipyridamole, 79% for dobutamine and 89% for dipyridamole-dobutamine echocardiography (p = NS for all). CONCLUSIONS: Routine dobutamine addition to dipyridamole stress testing is clinically useful and well tolerated. It expands the spectrum of the disease detectable by pharmacologic stress echocardiography and allows documentation of milder forms of coronary artery disease that can be missed by conventional dipyridamole or dobutamine stress echocardiography.

The atropine factor in pharmacologic stress echocardiography. Echo Persantine (EPIC) and Echo Dobutamine International Cooperative (EDIC) Study Groups.

OBJECTIVES: This study sought to compare, head to head, the two most popular pharmacologic stress echocardiographic tests--dipyridamole and dobutamine--with state of the art protocols in a large multicenter prospective study. BACKGROUND: In the continuing quest for ideal diagnostic accuracy, pharmacologic stress echocardiography has quickly moved over the years from low to high dose regimens and is currently performed with atropine coadministration. METHODS: Dobutamine (up to 40 microgram/kg body weight per min) plus atropine (up to 1 mg over 4 h) and dipyridamole (up to 0.84 mg/kg per min over 10 h) plus atropine (up to 1 mg over 4 h) stress echocardiography was performed on different days, in random order and within 1 week in 360 patients with chest pain syndrome. Thirteen different echocardiographic laboratories, all fulfilling quality control criteria for stress echocardiographic reading, contributed to the study. RESULTS: No major complications occurred during either test. The test was interrupted before achievement of predetermined end points for limiting side effects in 37 dobutamine-atropine and 7 dipyridamole-atropine stress echocardiographic studies (feasibility 90% vs. 98%, p < 0.01). Diagnostic accuracy was assessed in a subset of 110 patients with no obvious rest dyssynergy (akinesia or dyskinesia) who underwent coronary angiography independently of test results and within 1 week of testing. Significant coronary artery disease (> or = 50% diameter reduction in at least one major coronary vessel by quantitative coronary angiography) was found in 92 patients. Sensitivity for detection of coronary artery disease was 84% (77 of 92) for dobutamine-atropine and 82% (75 of 92) for dipyridamole-atropine stress echocardiography (p = NS), with a specificity of 89% (16 of 18) for dobutamine-atropine and 94% (17 of 18) for dipyridamole-atropine stress echocardiography (p = NS). A significant correlation was present between peak wall motion score index during dipyridamole-atropine and dobutamine-atropine stress echocardiography (r = 0.83, p < 0.0001). CONCLUSIONS: Dobutamine-atropine and dipyridamole-atropine stress echocardiography are safe and feasible, although submaximal studies are more frequent with dobutamine. The two stresses have comparable accuracy in the detection of angiographically assessed coronary artery disease, although dobutamine is marginally more sensitive and dipyridamole marginally more specific. Stratification of the ischemic response in the space domain is also comparable with the two stresses.

Identification of viable myocardium by dipyridamole-induced improvement in regional left ventricular function assessed by echocardiography in myocardial infarction and comparison with thallium scintigraphy at rest.

In patients with coronary artery disease and left ventricular impairment, the distinction between ventricular dysfunction due to myocardial fibrosis and postischemic, viable, although dys-synergic, myocardium has important clinical implications. Experimental studies have shown that dipyridamole can increase myocardial function in stunned segments, outlining a potential role of dipyridamole-induced functional recovery as an ultrasonic marker of myocardial viability. The aim of this study was to assess whether the increase of regional left ventricular function early during dipyridamole infusion in basally asynergic segments could identify viable myocardium recognized by rest injected, delayed (greater than 14 hours from tracer injection) thallium and (in a subset of patients) late functional recovery evaluated by a follow-up echocardiogram at rest. Twenty-two patients with angiographically documented coronary artery disease and regional dysfunction in resting conditions (average left ventricular ejection fraction 43 +/- 8%) were studied by echocardiography. All patients underwent a dipyridamole-echocardiographic test (up to 0.84 mg/kg over 10 minutes) and a delayed planar thallium study. A 13-segment model was used for both techniques. A score index ranging from 1 (normokinesia) to 4 (dyskinesia) was used for echocardiography. Thallium-201 activity was expressed in each segment as the percentage of maximal activity in the corresponding view. After dipyridamole, the wall motion score was assigned to each segment in resting conditions and at peak hyperkinesia before possible mechanical signs of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Value of rest thallium-201/technetium-99m sestamibi scans and dobutamine echocardiography for detecting myocardial viability.

The relation between radioisotopic and echocardiographic markers of myocardial viability and postrevascularization recovery of function is still to be defined. To this purpose, 14 patients (11 men, 3 women, aged 35 to 64 years, mean 54 +/- 7) with ventricular dysfunction were studied by a multiparametric approach. Each patient underwent, on separate days, rest thallium-201 and technetium-99m sestamibi scintigraphy, dobutamine echocardiography and coronary angiography. Coronary angiography was analyzed by a quantitative approach. Thallium uptake at rest was quantified from planar early (10-minute) and delayed (16-hour) thallium-201 images and expressed as a percentage of maximal activity in each projection using a 13-segment model. Sestamibi uptake was expressed in the same way. Dobutamine (up to 10 micrograms/kg/min) echocardiography was analyzed using a score index ranging from 1 (normokinesia) to 4 (dyskinesia) and a similar segmental model. Before revascularization 50 segments were grouped as normal (coronary stenosis < 50% and normal function, group 1); of the remaining 132 segments with > 50% coronary stenosis, 57 had normal wall motion (group 2) and 75 showed regional dyssynergies (group 3). Early and delayed thallium-201 regional percent activities did not differ in group 1 and in group 2 but were significantly less in group 3 segments. Sestamibi percent activity was more in group 1 and significantly reduced both in group 2 and 3 segments. Segments with improved wall motion after dobutamine had more early, delayed thallium-201 and sestamibi percent activities than unresponsive segments. Postrevascularization echocardiography was performed in all patients. Delayed thallium-201 scans and dobutamine echocardiography showed good sensitivity and specificity in detecting viable myocardium. (ABSTRACT TRUNCATED AT 250 WORDS)

Protective effect of nisoldipine on dipyridamole-induced myocardial ischemia: correlation with exercise electrocardiography.

BACKGROUND: Nisoldipine, a dihydropyridine calcium channel blocker with strong coronary dilatative action, is commonly used in the treatment of myocardial ischaemia; its beneficial effect on effort angina has been demonstrated by several previous reports. Infusion of dipyridamole in doses sufficient to provoke myocardial ischaemia in patients with significant coronary artery disease is used safely in imaging studies for diagnostic purposes. OBJECTIVE: To evaluate the potential effect of nisoldipine on dipyridamole-induced ischaemia and to compare the results with the effect of nisoldipine on exercise-induced ischaemia. METHOD: Twelve patients (10 men and two women, mean age 62 +/- 8 years) with significant coronary artery disease (at least 70% lumen reduction in at least one major coronary vessel) were selected for inclusion in the study. In accordance with the inclusion criteria, the patients exhibited an ischaemic diagnostic response to a multistage exercise electrocardiography stress test (> 0.15 mV ST segment depression compared with the resting electrocardiographic tracing) and to a dipyridamole-echocardiography test (transient left ventricular dyssynergy of contraction during infusion of dipyridamole up to 0.84 mg/kg over 10 min), after 3 days' cessation of antianginal treatment. After treatment with oral nisoldipine (10 mg twice daily) was introduced, the patients repeated the two tests, within 18 days of the first evaluation. RESULTS: The dipyridamole-echocardiography test was positive for ischaemia in 12 patients who were not receiving nisoldipine and in eight patients who were receiving the drug (100% and 67% respectively, P < 0.05). In the eight patients who gave positive dipyridamole-echocardiography tests both with and without treatment, dipyridamole time (time to onset of dyssynergy during the test) increased from 7.9 +/- 2.9 min to 10.2 +/- 3.1 min (P < 0.01). In these patients, no significant changes were observed, at ischaemia, in the severity and extent of induced dyssynergy, evaluated as wall motion score index (each of 16 left ventricular segments scored from 1 = normal to 4 = dyskinetic) after treatment (score variations from baseline to ischaemia: 0.20 +/- 0.11 without nisoldipine and 0.16 +/- 0.06 with nisoldipine; NS). Variations in dipyridamole time (arbitrarily considered to be 15 min in the negative dipyridamole-echocardiography test) were significantly correlated with variations in exercise time (duration of exercise to exhaustion or diagnostic positive response on the electrocardiogram): r = 0.75 (P < 0.01). No significant differences were recorded in rate-pressure product (beats/min x mmHg x 100) at peak ischaemia between patients who were or were not receiving nisoldipine, during either the exercise electrocardiography stress test (233 +/- 36 with nisoldipine and 244 +/- 39 without nisoldipine; NS) or the dipyridamole-echocardiography test (147 +/- 21 with nisoldipine and 133 +/- 30 without nisoldipine; NS). CONCLUSION: Nisoldipine treatment can protect from dipyridamole-induced ischaemia, being associated with a longer stress time, and completely preventing the development of ischaemia in some patients. The therapy-induced changes in ischaemic threshold during the dipyridamole-echocardiography test correlate with variations in exercise tolerance.

[Propafenone and flecainide in the therapy of ventricular arrhythmias]. / Il propafenone e la flecainide nella terapia delle aritmie ventricolari.

Flecainide and propafenone are antiarrhythmic drugs of the class 1C (Vaughan and Williams) commonly used for ventricular arrhythmias. The purpose of the present study was to evaluate the efficacy of these drugs in 170 consecutive patients with ventricular arrhythmias who referred to our cardiological ambulatory. The study population was divided into two groups according to the absence (group A,82 patients) or presence of organic heart disease (group 1B: 51 patients with left ventricular ejection fraction (LVEF) >35%; group 2B: 37 patients with LVEF<35%). Ventricular arrhythmias were evaluated with a 48 hours Holter monitoring at baseline, and with a control 24 hours Holter monitoring at 15 days (for optimizing the dosage), at 5 months and at 10 months from the beginning of antiarrhythmic therapy. Patients of group A were randomly assigned to antiarrhythmic treatment (flecainide 150-300 mg/die or propafenone 450-900 mg/die). For patients of group B, such choice was leaded by the clinical and strumental data (32 patients were treated with flecainide, 56 patients with propafenone). In the 160 patients who ended the 10 months follow-up, we observed the following results: patients of group A showed a mean percentage reduction in incidence of premature ventricular complexes (PVC) after therapy in comparison to basal conditions of 93% and 89% with flecainide and propafenone, respectively, after a treatment of 5 months (p < 0.001); after 10 months mean percentage reduction of PVC was 91% with each drug (p = n.s.); complex ventricular events (CVE) were reduced of 90% and of 100% after 5 and 10 months, respectively, of treatment with flecainide and of 100% both after 5 and 10 months of treatment with propafenone (p = n.s.) -- patients of group 1B showed a mean percentage reduction of PVC of 87% and 84% after 5 and 10 months, respectiively, of treatment with propafenone (p = n.s.); after 5 months of therapy mean percentage CVE reduction was 66% with flecainide and 86% with propafenone (p < 0.001); after 10 months this mean reduction was 53% with flecainide and 73% with propafenone (p < 0.001). -- patients of group 2B showed a mean reduction of PVC of 59% and 58% after 5 and 10 months of therapy with flecainide, and of 65% and 67% after 5 and 10 months of therapy with propafenone (p = n.s.); CVE were reduced of 28% with flecainide and of 47% with propafenone after 5 months of treatment (p < 0.001) and of 36% with flecainide against 52% with propafenone after 10 months (p < 0.01). In the present study there was no significant difference between the two drugs in terms of tollerance and collateral effects (8% with flecainide vs 7%, with propafenone). Our results confirm the efficacy of the 1C class drugs in the treatment of "essential" ventricular arrhytmias. This efficacy appears reduced in non selected patients with organic heart disease. In these latter patients propafenone has shown more efficacy than flecainide in reducing CVE.

Hyperkinetic ventricular arrhythmias in very elderly people with and without cardiac disease. Correlation with left ventricular echocardiographic parameters.

BACKGROUND: Morphological and functional changes induced by aging can hamper a clear distinction between pathological or paraphysiological phenomena in very old people. The incidence of hyperkinetic ventricular arrhythmias, for example, progressively increases in the elderly, even in the absence of overt cardiac disease. METHODS: One-hundred fifty-two clinically stable patients older than 80 years, submitted within 15 days to clinical evaluation, 24-hour continuous ambulatory ECG monitoring and echo Doppler examination, in the absence of antiarrhythmic treatment, were retrospectively selected in order to evaluate the incidence of ventricular arrhythmias, in patients with and without significant heart disease. The further aim of the study was to correlate the number of arrhythmias with left ventricular morphological and functional parameters, echocardiographically assessed. From the initial population, 80 patients (41 males, age 83 +/- 3 years) had significant heart disease (ischemic, hypertensive or valvular): Group I. Seventy-two patients (30 males, age 83 +/- 3 years) had no clinical or instrumental signs of heart disease: Group II. RESULTS: Considering echocardiographic data, Group I patients had a significantly higher left ventricular end-diastolic diameter (52 +/- 6 mm vs 47 +/- 4 mm, p < 0.01), lower ejection fraction (57 +/- 10% vs 64 +/- 6%, p < 0.01) and higher mass (275 +/- 84 g vs 208 +/- 46 g, p < 0.01), when compared with Group II. From ECG monitoring data, significant differences between the two groups were recorded in the incidence of premature ventricular beats per hour (79 +/- 163 vs 15 +/- 34, Group I vs Group II, p < 0.01) and presence of complex phenomena (couplets, triplets and runs: 51% vs 22%, p < 0.01). In old patients with documented cardiac disease a significant correlation was present between premature ventricular beats incidence and left ventricular end diastolic diameter (r = 0.39, p < 0.05) and left ventricular ejection fraction (r = 0.40, p < 0.05), while in patients without heart disease, no significant correlation was found between incidence of premature ventricular beats and echocardiographic morpho-functional parameters. CONCLUSIONS: In conclusion, hyperkinetic ventricular arrhythmias are globally frequent in old persons of very advanced age (more than 80 years), but, also in this subset, a significant distinction in terms of incidence and severity of arrhythmias is present between subjects with and without cardiac disease. A significant correlation between incidence of premature beats and non-invasive morpho-functional left ventricular parameters is present only for patients with overt heart disease.

Time-domain analysis of exercise-induced ST-segment elevation in Q-wave myocardial infarction: a useful tool for the screening of myocardial viability.

BACKGROUND: Exercise-induced ST-segment elevation in Q-wave leads has been traditionally associated with passive stretching of the infarct wall, perinecrotic ischemia and, according to recent scintigraphic studies, with myocardial viability. At present, however, no definitive conclusions are available. We evaluated the potential role of a time-domain analysis of exercise-induced ST-segment elevation for the identification of viable myocardium and residual ischemia in patients with previous Q-wave myocardial infarction. METHODS: Sixty patients with a previous Q-wave myocardial infarction underwent a bicycle exercise stress test, dobutamine stress echocardiography, coronary arteriography and left ventriculography. RESULTS: Patients with exercise-induced ST-segment elevation in Q-wave leads (n = 36) showed more severe impairment of resting left ventricular function, when evaluated in terms of wall motion score index at echocardiography (1.62 +/- 0.33 vs 1.41 +/- 0.22, p < 0.01) and in terms of wall motion score at ventriculography (5.9 +/- 1.6 vs 4.1 +/- 1.5, p < 0.03), compared to patients without ST-segment shift (n = 24). No differences between the two groups were seen in the severity and extension of coronary artery disease. The two groups of patients did not differ in the overall incidence of viability (50% in patients with vs 62% in those without ST-segment elevation, p = NS) and homozonal ischemia (39 vs 26%, p = NS), when evaluated with dobutamine echocardiography. However, a time-domain analysis of the ST-segment changes during exercise showed that the duration of exercise up to 0.1 mV ST-segment elevation was significantly lower in patients with viability (6.2 +/- 3.3 min) than in those without (10.2 +/- 2.2 min) (p < 0.001). Accordingly, ST-segment elevation occurred within 3 and 6 min of exercise in 7/18 and in 12/18 patients with viability respectively, but in only 0/18 (p < 0.01) and in 1/18 (p < 0.01) patients without viability. Thus, ST-segment elevation occurring within the first two stages of the exercise test was, respectively, 39 and 67% sensitive and 100 and 94% specific for viability. Early onset ST-segment elevation (within 3 and 6 min) was also more frequent in patients with high-dose dobutamine-induced homozonal ischemia than in those without (sensitivity for ischemia 50 and 67%; specificity 95 and 74%, respectively). CONCLUSIONS: After myocardial infarction, ST-segment elevation in Q-wave leads at the peak of exercise is associated with severe resting left ventricular dysfunction but fails to identify patients with a viable myocardium or residual ischemia. Instead, ST-segment elevation occurring in the early phases of exercise is a highly specific, although not very sensitive marker of dobutamine-assessed viability in the infarct area and may be indicative of residual ischemia.

Monitoring of cardiac output during exercise in coronary patients: a Doppler study.

The monitoring of aortic blood flow velocities by transcutaneous continuous-wave Doppler was performed in 45 patients to determine, non-invasively, the haemodynamic response to exercise in subsets of coronary patients during a multistage supine exercise tests. Group I consisted of 14 patients with ischaemia on effort (IE); group II, 12 patients with both IE and prior myocardial infarction (MI); group III, 19 patients with MI and no IE; there were also 12 normals. Peak flow velocity (PV) indices of cardiac output (CO), of peripheral resistance (PR) and of stroke work (SW) were measured every min. Resting CO was lower and PR higher in coronary patients than in normals. With exercise, for the same muscular work, CO increased less in IE patients (group I: y = 26.9 + 1.8 x cm sec-1; Group II: y = 21.9 + 1.8 x cm sec-1) than in MI (group III: y = 26.6 + 2.1 x cm s-1) and in normals (y = 35 + 2.7 x cm s-1) and PR decreased less. This suggested a more efficient distribution of CO towards working muscles. A shallower increase in SW was observed in all coronary patients in comparison with normals even if resting SW was significantly lower only in patients with MI (groups II and III). PV increased up to peak exercise only in group III, while it tended to plateau in ischaemic patients even earlier than IE occurred on the ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Ergonovine-echo test to assess the significance of chest pain at rest without ECG changes.

The aim of this study was to assess the feasibility and diagnostic role of ergonovine maleate infusion under continuous two-dimensional echocardiographic monitoring for the identification of vasospastic myocardial ischaemia in patients with chest pain at rest not associated with diagnostic ECG changes. One hundred and twenty-eight consecutive patients, selected on the basis of absence of ischaemic ECG changes during angina at rest before or during hospitalization, were enrolled in the study. Ergonovine maleate was i.v. administered in scaled doses (from 0.025 to 0.2 mg at 10 min intervals) under echocardiographic, electrocardiographic and systemic blood pressure monitoring. Wall motion asynergies were observed in 33 patients, accompanied by typical chest pain in 24 patients and by ECG changes in 25 (ST elevation in 13 patients, ST depression in seven, T wave changes in five). All patients were able to complete the test. Non life-threatening ventricular arrhythmias were observed in four patients exclusively in association with ischaemia. In seven patients with a positive test, coronary artery spasm was documented at angiography. In 16 patients with a positive test, the vasospastic event was reproduced by a hyperventilation-echo test or a second ergonovine maleate-echo test performed within 3 days of the first examination. In none of the patients with a negative test was documentation of myocardial ischaemia due to a primary reduction in coronary blood flow. Thus, in patients who do not show ECG changes during chest pain at rest, the ergonovine maleate-echo test is feasible and safe; it permits the recognition of ischaemic episodes on the basis of wall motion abnormalities when conventional 12-lead ECG-recorded chest pain is non-diagnostic.

Hyperventilation-echocardiography test for the diagnosis of myocardial ischaemia at rest.

The purpose of this study was to assess the feasibility, safety, specificity and sensitivity of the hyperventilation test performed under echocardiographic monitoring for the provocation of vasospastic ischaemia. Hyperventilation (approximately 30 cycles.min-1 for 5 min) was performed in 104 hospitalized patients, referred for pain typical of angina at rest, under 2-D echocardiographic and 12-lead electrocardiographic monitoring. All the tests were completed and no significant side effect was observed. In-hospital documentation of spontaneous myocardial ischaemia and/or ergonovine-induced ischaemia was achieved in 38 patients (group I). A positive hyperventilation-echocardiography test (occurrence of new transient asynergies or worsening of basal ones) was obtained in 32/38 patients. Among the group I patients, only 23 had diagnostic ST-T changes and only 16 experienced chest pain during the hyperventilation-echo test. Of the 66 patients without evidence of myocardial ischaemia at rest (negative ECG monitoring during hospitalization and/or negative ergonovine maleate-echo test)--Group II, none showed echocardiographic changes, seven presented ST-T changes and six complained of typical chest pain during the test. Thus, in relation to in-hospital documentation of myocardial ischaemia at rest, both spontaneous and/or ergonovine-induced episodes, the hyperventilation-echo test showed a specificity of 100%, a sensitivity of 84%, a positive predictive value of 100% and a negative predictive value of 92%. In conclusion, hyperventilation performed under echocardiographic monitoring is feasible and safe; it can be proposed as a screening test to unmask vasospastic myocardial ischaemia in patients with angina at rest, in whom documentation of spontaneous episodes is not available.

Myocardial viability: nuclear medicine versus stress echocardiography.

The failure of nonimaging techniques in the identification of myocardial viability has promoted the clinical application of radioisotopic and echocardiographic methods. Unfortunately, none of these techniques provides, per se, a 100% predictive accuracy and only few studies have been based on the postoperative improvement in regional wall motion, the absolute "gold standard" for myocardial viability. The recent thallium-201 protocols (reinjection, late redistribution, rest studies) have provided nuclear cardiology with a cell membrane integrity image able to unmask viable myocardium in more than 85% of viable segments. Sestamibi has been introduced as a nonrecirculating flow tracer able to detect transient ischemia as well as thallium-201. Its main limit, a high sensitivity to intermediate reductions in coronary blood flow, determines a high incidence of false positive studies. Positron emission tomography allows the evaluation of regional myocardial blood flow and metabolism. The marker of viable myocardium is the mismatch between reduced blood flow and normal or increased uptake of 18-F fluorodeoxyglucose. This technique allows the detection of viable tissue in most segments showing improved postoperative function. In our experience, applying a multiparametric approach, rest thallium-201 scan, rest sestamibi, dobutamine, and dipyridamole echocardiography showed a sensitivity and a specificity of 86%, 75%, 82%, 75% and 92%, 84%, 92%, and 89%, respectively, in the detection of residual viability. The main advantages of thallium-201 are reproducibility and standardization; those of stress echo are low cost and availability. In patients with severely depressed ventricular function, positron emission tomography retains a primary role when compared to thallium-201 and stress echocardiography.

Imaging of myocardial viability: a head-to-head comparison among nuclear, echocardiographic, and angiographic techniques.

The relationship between radioisotopic, echocardiographic, and angiographic markers of myocardial viability is still to be defined. To this purpose, 14 patients with previous myocardial infarction were studied using a multiparametric approach. Each patient underwent, on separate days, rest thallium 201 and technetium 99m Sestamibi planar scintigraphy, dobutamine/dipyridamole stress echocardiography, and coronary angiography; 11 of these patients underwent also dipyridamole echocardiographic testing. Thallium 201 and Sestamibi uptakes at rest were expressed as percentage of maximal activity in each projection using a 13 segment model. Dobutamine and dipyridamole stress echocardiography were analyzed using a score index ranging from 1 (normokinesis) to 4 (dyskinesis) and a similar segmentation. Coronary angiography was analyzed by quantitative approach. In all patients, follow-up echocardiography was performed following coronary revascularization. Before revascularization, 75 segments showed regional dyssynergies. Thallium 201 showed the highest sensitivity and specificity in the preoperative identification of viability, whereas Sestamibi was affected by a significant number of false-negative studies. Among echocardiographic techniques, dobutamine was slightly superior to dipyridamole in the detection of viable segments. The degree of coronary stenosis failed to predict the recovery of function following by-pass graft or angioplasty in almost all segments; however, in case of occlusion, most viable segments were perfused by adequately collateralized coronary arteries.