Stress echocardiography and the human factor: the importance of being expert.

The aim of this study was to evaluate how the diagnostic accuracy of a stress echocardiographic procedure, such as a dipyridamole echocardiography test, depends on the specific experience of the physician interpreting the test. Recordings of 50 consecutive dipyridamole echocardiographic tests were selected for the first part of the study. They were analyzed by 20 experienced echocardiographers with different backgrounds in stress echocardiography: 10 beginners (less than 20 stress studies interpreted with trained staff) and 10 experienced observers (greater than or equal to 100 stress studies performed). Diagnostic accuracy (true positive + true negative/total number of tests) versus the angiographic reference standard (greater than 70% coronary stenosis of at least one major coronary artery) was 62 +/- 6% for beginners and 85 +/- 3% for experienced observers (p less than 0.0001). In the second part of the study, 10 observers (5 beginners and 5 experienced observers) evaluated 2 different sets of 50 dipyridamole echocardiographic test studies before and after the training of the beginners. Before training, the accuracy of beginners was lower than that of experienced observers (61 +/- 7% versus 85 +/- 3%; p less than 0.001). After training, the accuracy gap was closed (83 +/- 3% versus 86 +/- 2%; p = NS). Therefore, interpretation of stress echocardiographic tests by an echocardiographer without specific training severely underestimates the diagnostic potential of this technique. One hundred stress echocardiographic studies are more than adequate to build the individual learning curve and reach the plateau of diagnostic accuracy that the test can yield.

High dose dipyridamole-echocardiography test in women: correlation with exercise-electrocardiography test and coronary arteriography.

The value of the exercise-electrocardiography test in detecting coronary artery disease in women is limited. Recently, the high dose dipyridamole-echocardiography test (two-dimensional echocardiographic monitoring during intravenous dipyridamole infusion, up to 0.84 mg/kg body weight over 10 min) was proposed as an alternative to exercise testing for the diagnosis of coronary artery disease. To establish the diagnostic usefulness of the exercise-electrocardiography and dipyridamole-echocardiography tests in this disease, the two tests were performed--on different days and in random order--in 83 consecutive women evaluated for a chest pain syndrome. All 83 women had taken no medications for greater than 48 h, and 15 had had a previous myocardial infarction. Positivity of the dipyridamole-echocardiography test was based on detection of a transient asynergy of contraction that was absent or of lesser degree at rest; the exercise-electrocardiography test (by upright cycloergometer) was considered positive when the ST segment was shifted greater than 0.1 mV 0.08 s after the J point. Coronary angiography showed significant coronary artery disease (greater than 70% luminal reduction of at least one major coronary vessel) in 39 women. No significant complications occurred in any patient during either test. Sensitivity and predictive value of a negative test were similar for the dipyridamole-echocardiography and the exercise-electrocardiography test (79 versus 72% and 84 versus 68%, respectively, whereas the dipyridamole-echocardiography test had greater specificity (93 versus 52%, p less than 0.001), accuracy (87 versus 62%, p less than 0.001) and a higher predictive value of a positive test (91 versus 57%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

High dose dipyridamole echocardiography test in effort angina pectoris.

The dipyridamole echocardiography test (intravenous dipyridamole with two-dimensional echocardiographic monitoring) was performed in 93 patients with effort chest pain and in 10 control subjects. The test was considered positive when regional asynergy appeared after dipyridamole administration. When negative at the low dose (0.56 mg/kg body weight in 4 minutes), the test was repeated on a different day with a higher dose (0.84 mg/kg in 10 minutes). All 93 patients underwent coronary arteriography; 72 of them had significant (greater than 70% luminal reduction) coronary artery disease. Thirty-eight of the 93 patients had a positive low dose dipyridamole echocardiography test; 15 other patients with a negative low dose test had a positive high dose test. All 53 patients with a positive test had significant coronary artery disease; 12 of them had a negative exercise stress test. In relation to the presence of coronary artery disease, the dipyridamole echocardiography test had an overall specificity higher than that of the exercise stress test (100 versus 71%) and a similar overall sensitivity (74 versus 69%). The dipyridamole echocardiography test is feasible in all patients with a good baseline echocardiogram. It detects the site of apparent ischemia more precisely than does an exercise stress test, and can unmask electrocardiographically silent ischemia. If performed in patients with a negative low dose dipyridamole echocardiography test, the high dose test adds sensitivity (probably by achieving maximal dilation in patients in whom the low dose is only partially effective), without any loss in specificity and with no apparent increase in risk.

Improved exercise capacity with acute aminophylline administration in patients with syndrome X.

The efficacy of the adenosine receptor blocker aminophylline on exercise capacity in patients with effort ischemia and documented coronary artery disease has been previously documented. In this study the effect of aminophylline on effort electrocardiographic (ECG) alterations and chest pain was tested in eight patients with syndrome X (anginal chest pain on effort, ischemic ECG changes during exercise, positive dipyridamole test, normal epicardial coronary arteries on angiography and absence of coronary spasm after ergonovine). After double-blind, randomized intravenous infusion of aminophylline (6 mg/kg body weight over 15 min) or placebo (20 ml of saline solution over 15 min), the eight patients with syndrome X underwent an upright bicycle exercise stress test on 2 consecutive days. After aminophylline, there was an increase in effort tolerance (aminophylline 7.7 +/- 1.2 min of exercise versus placebo 5.6 +/- 0.9, p less than 0.01) paralleled by an increase of the rate-pressure product (mm Hg x beats/min x 1/100) at 0.1 mV of ST segment depression or at peak exercise (aminophylline 278 +/- 55 versus placebo 230 +/- 24, p less than 0.05). Aminophylline provoked the abolition of ECG signs of ischemia in all eight patients. Thus, at a dosage that should effectively inhibit adenosine receptors, aminophylline infusion exerts a beneficial effect on exercise-induced chest pain and ischemia-like ECG changes in syndrome X. This effect occurs possibly through the prevention of myocardial flow maldistribution elicited by inappropriate adenosine release during effort in the presence of increased coronary resistance at the level of small intramural coronary arteries. This study, however, does not document the ischemic nature of effort-induced pain and ECG alterations in syndrome X.

Quantitative assessment of ultrasonic myocardial reflectivity in hypertrophic cardiomyopathy.

The purpose of this study was to investigate the relation between acoustic properties of the myocardium and magnitude of left ventricular hypertrophy in patients with hypertrophic cardiomyopathy. An on-line radio frequency analysis system was used to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and posterior free wall in 25 patients with hypertrophic cardiomyopathy and 25 normal age-matched control subjects. The integrated values of the radio frequency signal were normalized for the pericardial interface and expressed in percent. Tissue reflectivity was significantly increased in the hypertrophied ventricular septum, as well as in the nonhypertrophied posterior free wall, in patients with hypertrophic cardiomyopathy (58 +/- 15% and 37 +/- 12%, respectively) compared with values in normal subjects (33 +/- 10% and 18 +/- 5%, respectively; p less than 0.001). Furthermore, measurements of reflectivity of the septum or posterior free wall, or both, were beyond 2 SD of normal values in greater than 90% of the patients and were also abnormal in each of the five study patients who had only mild and localized left ventricular hypertrophy. No correlation was identified between myocardial tissue reflectivity and left ventricular wall thickness in the patients with hypertrophic cardiomyopathy (correlation coefficient r = 0.4; p = NS). These findings demonstrate that myocardial reflectivity is abnormal in most patients with hypertrophic cardiomyopathy and is largely independent of the magnitude of left ventricular hypertrophy. Moreover, quantitative analysis of ultrasonic reflectivity can differentiate patients with hypertrophic cardiomyopathy from normal subjects independently of clinical features and conventional echocardiographic measurements.

Transient myocardial dysfunction during pharmacologic vasodilation as an index of reduced coronary reserve: a coronary hemodynamic and echocardiographic study.

Regional coronary flow reserve and regional myocardial contractility were evaluated in 29 patients after maximal pharmacologic coronary vasodilation (intravenous dipyridamole, 0.56 mg/kg body weight, administered over 4 minutes). Nineteen patients had a severe (80 to 99%) proximal and isolated stenosis of the left anterior descending coronary artery and 10 patients had normal coronary arteries; all had normal ventricular function under rest conditions. Myocardial contractility was assessed by means of continuous two-dimensional echocardiographic monitoring; coronary reserve was evaluated by coronary sinus thermodilution. After dipyridamole infusion, 9 of the 19 patients with left anterior descending artery stenosis had transient myocardial asynergy involving the septum or apex, or both (Group IA), whereas 10 patients showed no asynergy (Group IB). No impairment of contractility was observed in the 10 patients with normal coronary arteries (Group II). Coronary blood flow was measured under basal conditions and up to 10 minutes after the end of dipyridamole infusion. In patients in Group II, dipyridamole induced an increase in great cardiac vein flow of 167 +/- 68% (mean +/- SD). The 10 patients in Group IB showed a response comparable with that of the control group (Group II) (136 +/- 45% increase in great cardiac vein flow; NS versus Group II), whereas the 9 patients in Group IA had an increase of 46 +/- 30% (p less than 0.01 versus both Group IB and Group II). No significant difference was found in the angiographic severity of the stenosis expressed in terms of minimal cross-sectional area (Group IA = 0.30 +/- 0.13 mm2, Group IB = 0.34 +/- 0.18 mm2; p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Quantitative texture analysis in two-dimensional echocardiography: application to the diagnosis of myocardial amyloidosis.

Qualitative and subjective analysis of two-dimensional echocardiographic images of the myocardial wall allows one to identify amyloid heart disease; the quantitative analysis of regional image texture might be an accurate method to differentiate normal from amyloid myocardial structures. To test this hypothesis, two-dimensional echocardiograms of nine normal subjects and six patients with histologically documented amyloid heart disease were evaluated. Quantitative texture measurements of the first order (mean gray level, skewness, kurtosis, energy and entropy) overlapped between the two groups. Among the second order statistics variables, entropy was significantly and consistently higher in amyloid versus normal patient data (septum in parasternal long-axis view: 6.3 +/- 0.3 versus 5.9 +/- 0.4; septum in apical four chamber view: 6.2 +/- 0.2 versus 5.8 +/- 0.3). Therefore, amyloid-involved myocardial walls show ultrasound image texture alterations that may be quantified with digital image analysis techniques.

Partitioning respiration of C3-C4 mixed communities using the natural abundance 13C approach--testing assumptions in a controlled environment.

Contributions of C3 and C4 plants to respiration of C3-C4 ecosystems can be estimated on the basis of their contrasting 13C discrimination. But accurate partitioning requires accurate measurements of the isotope signature of whole system respiratory CO2 (deltaR), and of its members (delta3 and delta4). Unfortunately, experimental determination of representative delta3 and delta4 values is virtually impossible in nature, generating a need for proxies (surrogates) of delta3 and delta4 values (e.g., the delta of leaf biomass). However, recent evidence indicates that there may be systematic differences among the delta of respiratory and biomass components. Thus, partitioning may be biased depending on the proxy. We tested a wide range of biomass- and respiration-based delta proxies for the partitioning of respiration of mixed Lolium perenne (C3) - Paspalum dilatatum (C4) stands growing at two temperatures inside large 13CO2/ 12CO2 gas exchange chambers. Proxy-based partitioning was compared with results of reference methods, including (i) the delta of whole plant respiratory CO2 (delta3 and delta4) or (ii) respiration rate of intact C3 and C4 plants. Results of the reference methods agreed near perfectly. Conversely, some proxies yielded erroneous partitioning results. Partitioning based on either the delta of shoot or root respiratory CO2 produced the worst bias, because shoot respiratory CO2 was enriched in 13C by several per thousand and root respiratory CO2 was depleted by several per thousand relative to whole plant respiratory CO2. Use of whole plant or whole shoot biomass delta gave satisfactory partitioning results under the constant conditions of the experiments, but their use in natural settings is cautioned if environmental conditions are variable and the time scales of respiration partitioning differ strongly from the residence time of C in biomass. Other biomass-based proxies with faster turnover (e.g., leaf growth zones) may be more useful in changing conditions.

In vitro identification of different degrees of mitral valve disease by online evaluation of radiofrequency ultrasound signal.

Sixty five mitral valves were studied in vitro with a 2.25 MHz transducer. Radiofrequency signals were analysed by a microprocessor system (implemented on an M-mode commercially available echocardiography) for online evaluation of ultrasonic backscatter (8 bits of amplitude resolution, 40 MHz sampling rate, 1 microsecond acquisition gate). The integrated value of the rectified signal amplitude was expressed as the integrated backscatter index (in db). The highest value recorded with ultrasonic scanning of each sample was taken as representative of that specimen. Calcification of mitral valves was assessed by radiography (24 mitral valves). Non-calcified mitral calves underwent pathological examination, and fibrotic valves (22 mitral valves) were differentiated from normal valves (19 mitral valves). A statistically significant (p less than 0.005) difference was recorded among the three groups for the index maximal value: calcific -7.4(3.1) db (mean(SD)), fibrotic -18.9(4.9) db, and normal -37.9(7.6) db. In conclusion, a microprocessor based system for online evaluation of radiofrequency ultrasonic signals, which may also be feasible for in vivo studies, provided a clear differentiation in vitro of calcific, fibrotic, and normal mitral valves.

ST segment depression elicited by dipyridamole infusion in asymptomatic hypertensive patients.

In asymptomatic patients with essential hypertension, electrocardiographic changes suggestive of myocardial ischemia can be elicited by rapid pressure lowering or by pronounced coronary arteriolar dilation. The aim of this study was to assess whether dipyridamole infusion might induce ischemic-like electrocardiographic changes in asymptomatic essential hypertensive patients and to describe the clinical and echocardiographic correlates possibly associated with this response. We therefore studied a control group of 20 normotensive individuals and a group of 28 asymptomatic patients with mild-to-moderate essential hypertension. All underwent dipyridamole-echocardiography testing (12-lead electrocardiogram and two-dimensional echocardiographic monitoring with dipyridamole infusion, 0.84 mg/kg over 10'). No patient showed transient regional dyssynergy during dipyridamole infusion. None of the normotensive and 10 of 28 of the hypertensive participants had horizontal or downsloping ST segment depression more than 0.1 mV during dipyridamole (0% versus 36%, p less than 0.01). Hypertensive patients with ("responders") (n = 10) and without ("nonresponders") (n = 18) ST segment depression showed similar values of percent fractional shortening in baseline conditions (32 +/- 5 versus 33 +/- 6, p = NS) and at peak dipyridamole infusion (45 +/- 8 versus 43 +/- 5, p = NS). The peak early to peak late velocity ratio values (evaluated from transmitral flow tracings by Doppler technique) were also similar in baseline conditions (0.86 +/- 0.14 versus 0.94 +/- 0.30, p = NS) and at peak dipyridamole (0.72 +/- 0.15 versus 0.78 +/- 0.32, p = NS).(ABSTRACT TRUNCATED AT 250 WORDS)

Normal ultrasonic myocardial reflectivity in hypertensive patients. A tissue characterization study.

Ultrasonic backscatter of myocardial walls is directly related to the morphometrically evaluated collagen content in humans. The integrated backscatter is also increased in hypertrophic cardiomyopathy, whereas it gives normal values in the physiological hypertrophy of elite athletes. We assessed the quantitatively evaluated myocardial reflectivity in 46 mild to moderate, clinically uncomplicated essential hypertensive patients, with echocardiographically assessed normal regional and global left ventricular function, and 22 age- and sex-matched normotensive control subjects. With an echo prototype implemented in our institute, we performed an on-line radiofrequency analysis to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and posterior wall. The integrated values of the radiofrequency signal of myocardial walls were normalized for those of the pericardial interface and expressed as a percent (integrated backscatter index). Hypertensive patients and control subjects differed in mean blood pressure (119 +/- 11 versus 95 +/- 5 mm Hg, p < 0.001) and left ventricular mass index (134 +/- 31 versus 105 +/- 21 g/m2, p < 0.001). However, integrated backscatter index overlapped for both the septum (28 +/- 17% versus 25 +/- 6%, p = NS) and the posterior wall (13 +/- 7% versus 13 +/- 4%, p = NS). In the hypertensive group, there was no detectable correlation between septal integrated backscatter index and either septal thickness (r = -0.26, p = NS) or mean arterial pressure (r = -0.14, p = NS). Hypertensive patients showed a normal pattern of quantitatively assessed ultrasonic backscatter, even in the presence of left ventricular hypertrophy.(ABSTRACT TRUNCATED AT 250 WORDS)

Dipyridamole echocardiography in essential hypertensive patients with chest pain.

The exercise-electrocardiography test shows limited feasibility and diagnostic accuracy for the noninvasive detection of coronary artery disease in hypertensive patients. Recently, the dipyridamole-echocardiography test (two-dimensional echocardiographic monitoring with dipyridamole infusion, up to 0.84 mg/kg over 10 minutes) has been proposed as an exercise-independent method for the diagnosis of coronary artery disease. The diagnostic usefulness of the exercise-electrocardiography test and the dipyridamole-echocardiography test was evaluated in 63 consecutive inpatients with history of chest pain, essential hypertension, and no previous myocardial infarction. The criterion of positivity for the exercise-electrocardiography test was a horizontal or downsloping ST segment shift exceeding 0.1 mV and for the dipyridamole-echocardiography test, a transient dyssynergy of contraction. Fifteen patients could not perform a diagnostic exercise-electrocardiography test because of an inability to exercise adequately (two patients), severe hypertension in spite of full antihypertensive therapy (six patients), or excessive blood pressure rise at the first step of the exercise-electrocardiography test (seven patients). Five patients could not perform the dipyridamole-echocardiography test because of a poor acoustic window. The overall feasibility was 76% for the exercise-electrocardiography test and 92% for the dipyridamole-echocardiography test (p less than 0.05). All 43 patients who performed both tests underwent coronary angiography; 30 had significant coronary artery disease (greater than 70% lumen reduction of at least 1 major coronary vessel). Sensitivity was 67% for both the exercise-electrocardiography test and the dipyridamole-echocardiography test (p = NS); specificity was 46% for the exercise-electrocardiography test and 92% for the dipyridamole-echocardiography test (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Prognostic value of pharmacologic stress echocardiography in patients with left bundle branch block.

PURPOSE: Although coronary artery disease is a frequent cause of left bundle branch block, the prognostic value of myocardial ischemia in patients with this conduction abnormality has not been defined. We investigated the value of pharmacologic stress echocardiography in risk stratification of patients with left bundle branch block. PATIENTS AND METHODS: Three hundred eighty-seven patients [230 men and 157 women, mean (+/- SD) age, 64 +/- 9 years] with complete left bundle branch block on the resting electrocardiogram underwent dobutamine (n = 217) or dipyridamole (n = 170) stress echocardiography to evaluate suspected or known coronary artery disease. A summary wall motion score (on a one to four scale) was calculated. The primary end points were cardiac death and nonfatal myocardial infarction. RESULTS: A positive echocardiographic result (evidence of ischemia) was detected in 109 (28%) patients. During a mean follow-up of 29 +/- 26 months, there were 21 cardiac deaths and 20 myocardial infarctions, 63 patients underwent coronary revascularization, and 1 patient received a heart transplant. In a multivariate analysis, four clinical and echocardiographic variables were associated with increased risk of cardiac death: resting wall motion score index [hazard ratio (HR) = 7.5 per unit; 95% confidence interval (CI), 2.8 to 20; P = 0.001], previous myocardial infarction (HR = 2.9; 95% CI, 1.1 to 7.3; P = 0.02), diabetes (HR = 2.7; 95% CI, 1.1 to 6.6; P = 0.03), and the change in wall motion score index from rest to peak stress (HR = 3.0 per unit; 95% CI, 1.0 to 8.6; P = 0.04). The 5-year survival was 77% in the ischemic group and 92% in the nonischemic group (P = 0.02). Four variables were associated with increased risk of cardiac death or infarction: previous myocardial infarction (HR = 3.4; 95% CI, 1.7 to 6.8; P = 0.0005), diabetes (HR = 2.4; 95% CI, 1.2 to 4.6; P = 0.01), resting wall motion score index (HR = 2.2 per unit; 95% CI, 1.1 to 4.1; P = 0.02), and positive echocardiographic result (HR = 2.2; 95% CI, 1.1 to 4.5; P = 0.03). The 5-year infarction-free survival was 60% in the ischemic group and 87% in the nonischemic group (P < 0.0001). Stress echocardiography significantly improved risk stratification in patients without previous myocardial infarction (P = 0.0001), but not in those with previous myocardial infarction (P = 0.08). In particular, it provided additional value over clinical and resting echocardiographic findings in predicting cardiac events among patients without previous infarction. CONCLUSIONS: Myocardial ischemia during pharmacologic stress echocardiography is a strong prognostic predictor in patients with left bundle branch block, particularly in those without previous myocardial infarction.

Lack of correlation between cardiac mass and arteriolar structural changes in mild-to-moderate hypertension.

A morphological restructuring of cardiac and arteriolar tissue is common in hypertension. The parallel evolution of these two processes as a compensatory response to pressure overload is a frequently assumed but unsubstantiated hypothesis. To evaluate this possibility, we have concomitantly measured left ventricular mass (LVM; two-dimensional echo) and minimal forearm vascular resistance (FVR; derived from the ratio of intra-arterial blood pressure: forearm blood flow by venous plethysmography) at maximal postischemic (13 min ischemia + 1 min hand exercise) reactive hyperemia. The study was performed on 29 essential hypertensive patients (15 males, 14 females, aged 50 +/- 10 years) who had not been undergoing treatment for hypertension for at least 15 days at the time of study. Minimum FVR was taken as a hemodynamic index of the integrated arteriolar lumen at the forearm level. LVM index and minimum FVR ranged from normal to clearly altered values. In spite of a wide spread of values, no correlation existed between the individual values of the two variables. Systemic mean blood pressure correlated with minimum FVR and tended to correlate with LVMI. Thus, morphological restructing of cardiac and arteriolar tissue does not seem to evolve in parallel in human hypertension. Pressure overload may contribute to cardiovascular hypertrophy, but other unrelated mechanisms may also underlie the development of cardiac and arteriolar abnormalities of human hypertension.

Regression of hypertensive myocardial hypertrophy does not affect ultrasonic myocardial reflectivity: a tissue characterization study.

OBJECTIVE: Ultrasonic backscatter from the myocardial walls is directly related to the morphometrically or biochemically evaluated collagen content in man, and shows a normal pattern of quantitatively assessed ultrasonic backscatter in hypertensive patients, even in the presence of left ventricular hypertrophy. Whether the pharmacologically induced regression of left ventricular hypertrophy in hypertensive patients is accompanied by a disproportionate increase in relative connective tissue content is not yet known. The objective of the present study was to assess the effects of regression of left ventricular hypertrophy on the quantitatively evaluated myocardial reflectivity in essential hypertensives. DESIGN: We evaluated 19 mild-to-moderate essential hypertensives with echocardiographically assessed left ventricular hypertrophy, before and after 8 months' effective antihypertensive therapy with 20-40 mg enalapril once a day, associated with diuretics or calcium antagonists, or both, in six patients to achieve optimal blood pressure control. Using a modified echo machine developed in the Institute of Clinical Physiology, Pisa, an on-line radio-frequency analysis was performed to obtain quantitative operator-independent measurements of the integrated backscatter signal of the ventricular septum and the posterior wall. The integrated values of the radio-frequency signal from the myocardial walls were normalized for those from the pericardial interface and were expressed as percentages (integrated backscatter index). RESULTS: In comparison with baseline, the treated hypertensives showed significant decreases in mean blood pressure, left ventricular mass index, and septal and posterior wall thickness. However, integrated backscatter index values were similar at baseline and after therapy for both the septum and the posterior wall. CONCLUSION: Antihypertensive therapy with enalapril does not increase myocardial reflectivity, although it does induce regression of left ventricular hypertrophy. This suggests that, in accord with experimental data, regression of hypertrophy is achieved by enalapril through a proportionate regression of the myocyte and connective tissue components of the myocardium.

Increased prevalence of ventricular arrhythmias in essential hypertensives with dipyridamole-induced ischemic-like S-T segment changes.

Essential hypertensives are at greater risk for ventricular arrhythmias than normotensive controls. A reduction in coronary flow reserve may be one of the mechanisms underlying this increased prevalence of ventricular dysrhythmias in hypertensives. It has previously been shown that dipyridamole infusion may provoke ischemic-like S-T segment depression in essential hypertensives with angiographically normal coronary arteries and reduced flow reserve. The aim of the present study was to assess whether electrocardiographic positivity (S-T segment depression greater than 0.1 mV from baseline) during dipyridamole testing (12-lead electrocardiogram and two-dimensional echomonitoring, with the infusion of 0.84 mg/kg dipyridamole over 10 min) might identify hypertensives at greater risk for ventricular dysrhythmias. We therefore studied 51 mild-to-moderate essential hypertensives by dipyridamole testing and 48-h Holter monitoring. All patients were off therapy for at least 2 weeks before testing and Holter evaluation. Left ventricular mass (by Penn convention) and ejection fraction (by Teichholtz rule) were evaluated by two-dimensional echocardiography. Lown classes 0-1 were found in 31 patients (Group 1) and Lown classes II-IV in 20 (Group 2). The two groups overlapped for mean blood pressure (121 +/- 9 versus 124 +/- 8 mmHg), left ventricular mass index (120 +/- 27 versus 141 +/- 42 g/m2) and left ventricular ejection fraction (54 +/- 6 versus 52 +/- 6). An electrocardiographically-positive dipyridamole test was found in seven of Group I and 16 of Group II patients (23 versus 80%, P less than 0.01). No patient showed a transient, either regional or global, systolic dysfunction during dipyridamole testing.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Usefulness of a high-dose dipyridamole-echocardiography test for diagnosis of syndrome X.

This study assesses whether the high-dose dipyridamole-echocardiography test (DET, 2-D echocardiographic and 12-lead electrocardiographic monitoring during dipyridamole infusion, up to 0.84 mg/kg over 10 minutes) can help to identify patients with syndrome X. DET was performed in 10 control subjects (group A) and in 19 patients with syndrome X (group B). Patients in group B had chest pain on effort, a positive exercise stress response (more than 0.1 mV of ST-segment depression), negative ergonovine test response and normal left ventricular function and coronary angiographic findings. During DET no subject in group A showed transient asynergy or ST-segment depression and none had chest pain; in group B, no patient had transient asynergy, 13 (68%) had chest pain and 16 (84%) had more than 0.1 mV of ST-segment depression. Percent fractional shortening was not significantly different in the 2 study groups, either basally (group A, 35 +/- 7; group B, 37 +/- 8) or at peak hyperkinesia during DET (group A, 48 +/- 8; group B, 54 +/- 10). Thus, dipyridamole-induced chest pain and ST-segment depression in patients with syndrome X are not associated with impaired regional or global left ventricular function. This entity of echocardiographically silent myocardial ischemia during DET may be a clue to noninvasive detection of syndrome X.

Usefulness of the dipyridamole-exercise echocardiography test for diagnosis of coronary artery disease.

To test the hypothesis that a dipyridamole infusion might sensitize the myocardium to exercise-induced ischemia, 33 patients with effort chest pain syndrome--including 24 with and 9 without angiographically documented coronary artery disease (CAD)--and 10 control subjects were studied. As inclusion criterion, all enrolled subjects had a negative resting high-dose dipyridamole-echocardiography test result for both mechanical (development of a transient asynergy) and electrocardiographic (greater than 0.1 mV ST-segment shift) changes. All performed 2 supine exercises during 2-dimensional echocardiography and 12-lead electrocardiography monitoring, immediately after high-dose (0.84 mg/kg over 10 minutes) dipyridamole (dipyridamole-exercise stress test) or placebo (exercise stress test) infusion. The overall sensitivity (by electrocardiographic, echocardiographic or combined criteria) for CAD detection was 10 of 24 for exercise stress test and 21 of 24 for dipyridamole-exercise stress test (42 vs 88%, p less than 0.01). The specificity was 19 of 19 for exercise stress test and 18 of 19 for dipyridamole-exercise stress test (100 vs 95%, difference not significant). Both exercise stress test and dipyridamole-exercise stress test yielded negative results in the 10 control subjects, with a similar peak rate-pressure product (X 1/100) reached in the 2 tests (287 +/- 55 vs 274 +/- 42, difference not significant). Eight patients (all with significant CAD) had positive results of their exercise stress test and all 8 had also positive dipyridamole-exercise stress test results, at a significantly lower rate-pressure product with respect to the exercise stress test (253 +/- 49 vs 204 +/- 35, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Different degrees of ischemic threshold stratified by the dipyridamole-echocardiography test.

Dipyridamole-echocardiography (echo) testing, exercise stress testing and coronary arteriography were performed in 141 patients with effort chest pain. Patients were separated into 5 groups according to the dose of dipyridamole needed to induce ischemia (0.56 mg/kg over 4 minutes vs 0.84 mg/kg over 10 minutes) and to the time of onset of the asynergy with the small dose (within vs beyond 3 minutes after the end of dipyridamole administration): group 1--early positive response to a small dose (33 patients); group 2--late positive response to a small dose (29 patients); group 3--negative response to a small dose, positive response to a large dose (17 patients); group 4a--negative response to both large and small doses, with significant coronary artery disease (CAD) (32 patients); and group 4b--negative response to small and large doses, without CAD (30 patients). All patients in groups 1, 2 and 3 had significant CAD. The rate-pressure product on exercise stress testing was measured at 0.10 mV of ST-segment shift in patients with a positive response and at peak exercise in patients with a negative response. Rate-pressure product significantly separated group 1 and group 2 from each other (157 +/- 46 and 229 +/- 33 mm Hg X beats/min X 1/100, respectively, mean +/- standard deviation) and from group 3, group 4a and group 4b (284 +/- 40, 290 +/- 51, and 298 +/- 45 mm Hg X beats/min X 1/100); values in the 3 latter groups overlapped.2+ Thus, the dipyridamole-echo test can stratify groups of patients with different levels of ischemia threshold on effort.