Normal Coronary Arteriography Research Articles

Torsades de Pointes in an Elderly Patient with “Broken Heart Syndrome”

Broken heart syndrome, also called transient left ventricular apical ballooning syndrome (TLVABS), is described as an acute cardiomyopathy characterized by acute, but rapidly reversible, left ventricle systolic dysfunction in the absence of atherosclerotic coronary artery disease which appears to be triggered by intense psychological and physical stress. The syndrome is also named takotsubo syndrome, ampulla cardiomyopathy, or stress-induced cardiomyopathy. We report a woman aged 75 years with dyspnea, ST-segment elevation in the precordial leads, elevation of cardiac enzymes, and normal coronary arteriography. Transient apical systolic left ventricular dysfunction and pneumonia were suspected. Gradual prolongation of QT interval and torsades de pointes (TdP) subsequently occurred. Patients had a complete recovery of cardiac function, normalization of QT interval, and normal apical cardiac wall motion in a few days after lidocaine pump and empiric antibiotics use. Since TdP is rarely reported with TLVABS, we should pay more attention to postmenopausal women with chest pain and elevated cardiac enzymes. We should keep TLVABS in mind and use convenient tools, such as bedside echocardiography, for diagnosis.

Extracorporeal life support in a severe Taxus baccata poisoning

Introduction. Yew (Taxus baccata) is a conifer known to be toxic since ancient times. Taxine A and taxine B, the toxic alkaloids of Taxus, block cardiac sodium and calcium channels causing nausea, vomiting, abdominal pain, cardiac arrhythmias, respiratory distress, coma, seizures, and death in yew poisoning. Case report. A 44-year-old male farmer was admitted to the hospital because of a suspected myocardial infarction. First bradycardia and then ventricular tachycardia were present and a severe right ventricular dilatation with biventricular dysfunction was observed but with normal coronary arteriography. He was resistant to conventional therapy and, 6 h after hospital admission, extracorporeal support with membrane oxygenation was applied. The patient recovered. Nine days later, a large number of yew leaves were unexpectedly observed in his feces. Botanical and laboratory analysis confirmed the poisoning. Blood (651 ng/mL) and urinary (5.6 mcg/mL) levels of 3,5-dimethoxyphenol (metabolite of taxicatine) were greater than previously reported in lethal cases. The patient was transferred to a psychiatric unit 17 days after admission. Conclusions. Intensive treatment of severe cardiovascular symptoms with antiarrhythmic drugs, temporary pacemaker, intra-aortic balloon pump, extracorporeal membrane oxygenation, and extracorporeal life support can be life-saving even after a potentially lethal ingestion of T. baccata leaves.

Feocromocitoma con consecuencias fatales. ¿Qué podemos aprender de este caso?

Describimos el caso de un paciente de 42 años que desarrolló shock cardiogénico con elevación de enzimas cardíacas y coronariografía normal, cuyo diagnóstico final fue feocromocitoma. El paciente tuvo una evolución tórpida con fracaso multiorgánico y necesidad de intubación orotraqueal, balón de contrapulsación y hemodiafiltración continua. Finalmente tuvo hematoma parenquimatoso cerebral con deterioro neurológico irreversible. Además destacamos el papel de la ecografía abdominal en el diagnóstico de feocromocitoma en pacientes críticos. The case of a 42-year old male patient diagnosed of adrenal pheochromocytoma who developed cardiogenic shock, with increased cardiac enzymes and normal coronary arteriography is described. The patient had a torpid clinical course with multiorgan failure and was treated with tracheal intubation, balloon contrapulsation and continuous hemodiafiltration. Finally, he had intracerebral hematoma with irreversible neurologic damage. We highlight the value of abdominal ultrasonography in the diagnosis of pheochromocytoma in critical patients.

Baseline Clinical Characteristics and Midterm Prognosis of STE‐ACS and NSTE‐ACS Patients with Normal Coronary Arteries

We sought to compare clinical profiles and midterm prognosis of patients with normal coronary arteries presenting with ST-elevation ACS (STE-ACS) versus non-ST-elevation ACS (nSTE-ACS). There are limited data regarding ACS in patients with normal coronary arteries, and especially clinical differences between ST-ACS and nSTE-ACS patients have not been evaluated sufficiently. The study group comprised 190 patients (mean age: 53.2 years, 63.1% males, 63.6% STE-ACS) presenting with ACS and normal coronary angiograms. The participants were evaluated in terms of 42 clinical variables. MACE [cardiac death (CD) and hospitalization for angina (HA)] were the study end points. STE-ACS in comparison to nSTE-ACS patients were younger (P < 0.01), were more frequently males (P < 0.01), had more often infection prior to ACS (P < 0.01), higher hsCRP on admission (P < 0.01), and greater infarct size, measured by maximal troponin I (P < 0.01). By multivariate analysis in this subgroup, predictors of outcome were hsCRP (P = 0.03) and raised troponin I (P = 0.02). nSTE-ACS in comparison to STE-ACS patients were more obese (BMI, P < 0.01), had higher LDL cholesterol (P < 0.01), fasting glucose (P = 0.03). LDL cholesterol (P = 0.02) and fasting glucose (P = 0.03) emerged as independent predictors of outcome in these patients. Mean follow-up period was 25.4 months. STE-ACS patients had twice fewer MACE rate than nSTE-ACS patients [(1-CD, 12-HA; 11%) vs (1-CD, 16-HA; 25%), respectively, log rank P < 0.01]. STE-ACS and nSTE-ACS patients with normal coronary arteriography have different clinical profiles. In nSTE-ACS patients more pronounced metabolic abnormalities were identified, while in STE-ACS patients inflammatory background was more significant.

Accident coronarien aigu révélé par un œdème pulmonaire survenu en plongée sous-marine

We report the case of a 64-year-old healthy male diver who presented an unusual diving-related pulmonary edema induced by a painless myocardial infarction with normal coronary arteriography. We review the related literature and discuss the pathophysiologic mechanisms that would contribute to provoke this myocardial injury during diving.

Mid‐Ventricular Ballooning Heart Syndrome

Stress cardiomyopathies have been increasingly reported these last years, especially in women as a transient left ventricular apical ballooning syndrome. We report six cases in whom, in the context of anxious situations, echocardiograms and ventriculographies revealed mid-ventricular akinesis with preservation of apical and basal contractilities with normal coronary arteriography. This "mid-ventricular ballooning heart syndrome " should probably be classified as a new type of heart stress related syndrome.

Acute Coronary Syndromes Associated With Thrombus in the Sinus of Valsalva and Normal Coronary Arteriography: The Pivotal Role of Transesophageal Echocardiography in the Intensive Care Unit

We describe 4 patients with thrombus in nonaneurysmal sinus of Valsalva. The diagnosis was made with transesophageal echocardiography performed in the Intensive care unit, in the setting of acute coronary syndromes. Coronary arterlography showed normal coronary arteries in each patient. In 3 patients, conservative medical therapy resulted in full recovery. Two patients had previously undergone aortic valve surgery.

Heart Rate Variability in Patients with Systemic Sarcoidosis

The identification of subjects with systemic sarcoidosis at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death in various conditions. Therefore, the aim of the study was to evaluate HRV in patients with systemic sarcoidosis. The study included 35 patients with biopsy proven systemic sarcoidosis who were not taking antiarrhythmic medications. Thallium scintigraphy was performed to all patients with systemic sarcoidosis. The cardiac sarcoidosis was accepted in 16 patients as abnormal thallium scintigraphy and normal coronary arteriography. The time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Twenty-four healthy subjects represented a control group for HRV analysis. There were no differences in age (44 +/- 13 years for cardiac sarcoidosis, 42 +/- 15 years for noncardiac sarcoidosis, and 40 +/- 10 years for control group; P = NS), sex (the ratio of female; 63%, 68%, and 55%, respectively; P = NS), and echocardiographic ejection fraction (63 +/- 10%, 67 +/- 8%, and 69 +/- 6%, respectively; P = NS) among study groups. The mean SDNN value of the group with cardiac sarcoidosis was significantly lower than both the group with noncardiac sarcoidosis and the control group (72 +/- 32 ms vs 110 +/- 46 ms and 152 +/- 36 ms; P < 0.05, respectively). HRV is decreased in patients with systemic sarcoidosis compared to the control group. This decreasing is more obvious in patients with cardiac sarcoidosis.

QT Dispersion in Sarcoidosis

QT dispersion (QTd) is the maximal interlead difference in QT interval on surface 12-lead ECG. An increase in QTd is found in various cardiac diseases. Sarcoidosis augments inhomogeneity in ventricular repolarization by sarcoid granuloma, which significantly correlates with ventricular fibrillation. Changes in QTd in the course of sarcoidosis have not been investigated previously. The study included 35 patients with systemic sarcoidosis. The diagnosis of systemic sarcoidosis was made by biopsy. Thallium scintigraphy was performed in all patients with systemic sarcoidosis. Cardiac sarcoidosis was diagnosed in 16 patients based on abnormal thallium scintigraphy and normal coronary arteriography results. QTd, corrected QTd (cQTd), maximum QT (QTmax), maximum corrected QT (cQTmax), minimum QT, and minimum corrected QT intervals were measured. Twenty-four healthy subjects represented the control group for QT interval analysis. In the cardiac sarcoidosis group, mean QTd (+/- SD) was significantly greater than in the noncardiac sarcoidosis group and control group (49.50 +/- 10.86 ms, 28.14 +/- 11.02 ms, and 27.08 +/- 10.41 ms, respectively; p < 0.001). cQTd was significantly greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group and control group (53.17 +/- 10.44 ms, 30.61 +/- 10.94 ms, and 29.01 +/- 10.52 ms, respectively; p < 0.001). QTmax (440 +/- 15.01 ms, 409 +/- 14.86 ms, and 410 +/- 13.21 ms; p < 0.001) and cQTmax (449 +/- 16.31 ms, 417 +/- 12.51 ms, and 418 +/- 11.76, respectively; p < 0.001) were also significantly greater in patients with cardiac sarcoidosis. In a limited follow-up group (11 cardiac and 9 noncardiac sarcoidosis patients), the incidence of premature ventricular contraction (PVC) on ECG was greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group (36% and 0%, respectively; p < 0.05). A medium correlation existed between QTd and PVC (r = 0.331, p < 0.05). QTd, cQTd, QTmax, and cQTmax are prolonged in patients with cardiac sarcoidosis compared to the patients with noncardiac sarcoidosis and control subjects. The incidence of PVC on ECG was greater in the cardiac sarcoidosis group than in the noncardiac sarcoidosis group.

Cardiovascular outcome of patients with abnormal coronary vasomotion and normal coronary arteriography is worse in type 2 diabetes mellitus than in arterial hypertension: A 10 year follow-up study

Diabetes and arterial hypertension are major cardiovascular risk factors. Coronary endothelial dysfunction is frequently observed in diabetic and hypertensive patients. This study was designed to compare cardiovascular outcome of hypertensive (HT) and type 2 diabetic patients (D2) with angiographically normal coronary arteries on the basis of their epicardial coronary endothelial function. Coronary reactivity assessment by cold-pressor test (CPT) using quantitative coronary angiography was achieved in 65 HT (45 males, 20 females) aged 51.9+/-7.6 years, and in 59 D2 (32 males, 27 females) aged 48.9+/-7.3 years, with angiographically normal coronary arteries and without other major coronary risk factor. Cardiovascular events (CVE) were recorded with a mean follow-up of 108+/-15 months in HT, and 113+/-10 months in D2. During CPT, in HT coronary artery dilation occurred in 10.8% of the patients, no change in 21.5%, and constriction in 67.7%. In D2, dilation occurred in 3.4% of the patients, no change in 18.6%, and constriction in 78.0%. During follow-up, in HT there were nine CVE in 6/65 patients (9.2%), all in the 6/44 (13.6%) patients with coronary artery constriction. In D2, there were 18 CVE in 16/59 patients (27.1%, P<0.01 versus HT), with 17 CVE in the 15/46 patients with coronary artery constriction, and one CVE in the 1/13 patients without constriction (32.6% versus 7.7%). In patients with coronary artery constriction, CVE were more frequent in D2 than in HT (P<0.05). Last, CVE were more severe and occurred earlier in D2 than in HT. In conclusion, epicardial coronary endothelial dysfunction is predictive of long-term CVE in HT and D2 with angiographically normal coronary arteries. Cardiovascular outcome of patients with coronary constriction is worse in D2 than in HT. At the opposite, patients without constriction have good cardiovascular prognosis in both subgroups.

Mortality in patients with microvascular disease.

Patients with chest pain/ischemic cardiac disease and normal coronary arteriography are thought to have a benign prognosis despite diminished quality of life. Many patients with hypertension fall into this group, at least in the early stage of their disease. Whether abnormalities in coronary flow reserve in these patients are associated with increased morbidity and mortality is unknown. One hundred sixty-eight patients with chest pain/ischemic cardiac disease and normal coronary angiograms who underwent invasive measures of coronary flow reserve were followed longitudinally. Mortality and quality of life were ascertained by query of the national death index and telephone administration of standardized questionnaires. Patient follow-up occurred at a mean of 8.5 years. In the abnormal coronary flow reserve group, 12 deaths (20%) were documented in 60 patients compared with eight out of 108 patients (7%; p=0.016) with normal coronary flow reserve. Coronary flow reserve did not predict impairment in functional health status in long-term follow-up. Thus, invasive measures of coronary flow reserve in patients with chest pain/ischemic cardiac disease and normal coronary angiograms predicted increased mortality. Surviving patients with chest pain/ischemic cardiac disease and normal coronary angiograms have significant morbidity.

Nitric oxide in ischemic heart disease. Defective production or impaired function?

Among the mediators released by coronary arterial endothelium, namely prostacyclin, endothelin, thrombomodulin, and so on, nitric oxide (NO) (i.e. endothelial-derived relaxing factor) has been the subject of our intense research. A biologic link between endothelial damage and atherosclerotic coronary arterial disease has been presumably related to decreased arterial bioavailability of NO through predisposing to leucocyte and platelet adhesion, vasoconstriction and smooth muscle cell proliferation. The present study is intended to re-evaluate the potential role of NO in the pathophysiology of coronary heart disease through assessing the serum NO metabolites (nitrites and nitrates) in 150 patients (patients) with ischemic heart disease (118 male, 32 female; mean age 53.4 ± 8.3 years, range 33–80 years). Of the latter, 77 patients (51.3%) had unstable angina (AP), and 73 (48.7%) had recent myocardial infarction (MI). Twenty subjects with normal coronary arteriography (15 male, 5 female; mean age 55.4 ± 4.5 years) served as a control group. Of the studied patients, 89 (59%) were smokers, 68 (45%) were diabetics, 60 (40%) were hypertensives and 63 (43%) were dyslipidemic. Following clinical evaluation including 12-lead ECG, all patients were subjected to routine laboratory testing (including liver and kidney functions, lipid profile, CBC, and random blood sugar). Specific laboratory tests included serum fibrinogen and plasma NO expressed as its metabolites, nitrites and nitrates (NOx), as measured by the Griess reaction. All patients and controls were subjected to diagnostic coronary arteriography with assessment of the extent of coronary disease (number of affected vessels) as well as the severity of stenosis (using the Gensini scoring system). Compared with the control group, ischemic patients had significantly lower levels of NOx (52.8 ± 7.3 vs 15.8 ± 7.3, P < 0.000) with a significantly lower level of NOx in the MI group compared with the AP group (22.1 ± 3.4 vs 9 ± 2.3, P < 0.000). No significant correlation either with the extent or the severity of coronary artery disease was shown. Furthermore, compared with nonsmokers, smokers with ischemic heart disease exhibited significantly lower levels of serum NOx (28.5 ± 14.2 vs 13.8 ± 10.3, P < 0.002). Other risk factors (dyslipidemia, hypertension, diabetes mellitus [DM]) in the ischemic group did not show any significant correlation with serum NOx level (P = 0.1, P = 0.09, P = 0.1, respectively). In conclusion, although NO plays a major role in mediating coronary arterial dilation under healthy condition, it is substantially defective in coronary arterial disease, yet the poor correlation with DM and dyslipidemia (diseases primarily characterized by endothelial dysfunction) would point to impaired NO function rather than just defective production.

Resting “Solar Polar” map pattern and reduced apical flow reserve: characteristics of apical hypertrophic cardiomyopathy on SPECT myocardial perfusion imaging

Patients with apical hypertrophic cardiomyopathy (ACM) are often referred for myocardial perfusion single photon emission computed tomography (SPECT) as a result of marked T-wave inversion and chest pain syndromes. Stress perfusion defects have been reported in ACM, but the characteristic SPECT pattern as well as the typical findings on volume-weighted polar maps has not been described. Dual-isotope rest (thallium 201) and exercise or adenosine stress (technetium 99m tetrofosmin) myocardial perfusion SPECT was performed in 11 patients with ACM, including 8 with either normal coronary arteriography (n = 5) or a low pretest probability of coronary artery disease (CAD) (n = 3), and 14 control patients with concentric left ventricular hypertrophy. An 8-pixel-diameter circular region of interest was used to quantitatively compare apical and septal counts on CEqual volume-weighted polar maps. A characteristic "Solar Polar" map pattern resulting from the increased apical counts was present in each ACM patient at rest, with a mean apical-septal ratio of 1.39 +/- 0.17 (range, 1.23-1.62, P <.01 vs concentric left ventricular hypertrophy group). With stress, there was a significant decrease in the apical-septal ratio (0.96 +/- 0.18, P <.001 vs rest) in the ACM subgroup without CAD. Patients with ACM demonstrate a newly described "Solar Polar" map pattern at rest, as well as relative apical ischemia on the stress images even in the absence of CAD.

Atrial septal defect and myocardial infarct

The etiology for an acute myocardial infarction with normal coronary arteriography should rule in and rule out the presence of an atrial septal defect. Acute increases in left to right shunting with an atrial septal defect may lead to episodes of myocardial necrosis and right ventricular dysfunction. This case report describes such a scenario.

Cardiomyopathie de stress : à propos de deux cas

The authors reported two cases of acute catecholamines cardiomyopathy expressed clinically by chest pain and dyspnea, without any previous cardiac history. The diagnosis of human stress cardiomyopathy is established on: typically rapid onset aftermath of intense emotional stress, left ventricular apical akinesis and hyperkinetic motion of basal walls imaged by two-dimensional echocardiography. Rapid reversal clinical course and normal coronary arteriography. Similar finding have been observed in conjunction with pheochromocytoma who have been excluded by normal levels of urinary catecholamines metabolites.

Prevalence of factor V Leiden (APCR) and other inherited thrombophilias in young patients with myocardial infarction and normal coronary arteries

ObjectiveTo investigate the role of activated protein C resistance (APCR, factor V Leiden) in coronary artery thrombosis.MethodsThe prevalence of APCR and of congenital deficiencies of antithrombin III, protein C, protein...

False positive ST-segment depression during exercise in subjects with short PR segment and angiographically normal coronaries: Correlation with exercise-induced ST depression in subjects with normal PR and normal coronaries

The aim of this study was to investigate exercise-induced ST-segment depression in subjects with a 120-ms or shorter PR segment and normal coronary arteries. A population of 86 individuals who demonstrated ST-segment depression of 1.5 mm or more on treadmill testing and had a subsequent normal coronary arteriography was classified into two groups. Group A (n = 71) comprised those with a normal PR interval on baseline electrocardiogram 160.9 +/- 14.8 ms (mean +/- 1 SD), and group B (n = 15) comprised those with a 120-ms or shorter PR interval 113 +/- 8.8 ms (mean +/- 1 SD). All subjects had undergone a symptom-limited treadmill test by the standard Bruce protocol (mainly for evaluation of chest pain or angina-like pain), during which they demonstrated ST depression of 1.5 mm or more in either lead II, lead V2, or lead V5. All had normal or near normal coronary arteries on angiography. In the subjects with short PR segments and angiographically normal coronaries, a trend of greater ST-segment depression during treadmill testing as compared with control subjects was observed in lead V5. In the same group, ST-segment depression at the 9th minute of exercise was more prevalent in lead V5 than in lead II or V2.

Coronary vascular reserve is similarly reduced in hypertensive patients without any other coronary risk factors and in normotensive smokers and hypercholesterolemic patients with angiographically normal coronary arteries

Hypertensive patients (HTP) with left ventricular hypertrophy have reduced coronary vascular reserve (CVR), but in HTP without left ventricular hypertrophy, CVR is within the normal range according to values determined in subjects without taking into account coronary risk factors such as cigarette smoking or hypercholesterolemia. To examine the influence of hypertension, cigarette smoking, and hypercholesterolemia on coronary flow and resistance reserve, coronary flow velocity was measured using a Doppler catheter before and after a maximally vasodilating dose of papaverine in 15 normotensive subjects without any coronary risk factors (Group 1), in 12 nonsmoker HTP with normal lipid profiles who had never been treated (Group 2), in 8 normotensive smoker patients (Group 3), in 9 normotensive nonsmoker patients with hypercholesterolemia (Group 4), and in 13 normotensive smoker patients with hypercholesterolemia (Group 5). All patients had normal coronary arteriography and left ventricular mass and function. Peak-to-resting coronary flow velocity ratio and mean aortic pressure were used to determine coronary flow reserve (CFR) and a minimal coronary vascular resistance index (MCVRI). Results show that in groups 2, 3, 4, and 5 comparatively to Group 1, CFR was similarly reduced (4.60 +/- 0.74 [P < .001], 4.59 +/- 0.35 [P < .001], 5.01 +/- 0.55 [P < .05], 5.03 +/- 0.78 [P < .05], groups 2 to 5, respectively, compared to group 1 5.66 +/- 0.68), and that MCVRI was similarly augmented (0.19 +/- 0.03 [P < .01], 0.20 +/- 0.0 [P < .001], 0.19 +/- 0.02 [P < .05], 0.19 +/- 0.03 [P < .05], groups 2 to 5, respectively, compared to group 1 0.16 +/- 0.02). In conclusion, HTP without left ventricular hypertrophy have a similar reduction of their CVR as smokers and hypercholesterolemic patients when compared to a group of subjects without any coronary risk factors. This should be taken into account when determining a group of control subjects for coronary reserve.

Hyperinsulinaemia in Syndrome X: A Marker of the Syndrome?

Stimulated hyperinsulinaemia is observed in some patients with syndrome X, defined as angina, positive stress test and normal coronary arteriography, and may be involved in the pathogenesis of the syndrome. An increased sympathetic response to exercise may also be pathogenetically involved. However, the diagnostic value of hyperinsulinaemia as a marker of this syndrome has not been defined. We determined blood glucose and immunoreactive insulin during fasting, at 60 and 120 min after a glucose load of 75g in 21 patients (eight men, 13 women, 53.9 +/- 7.1 years old) with syndrome X and in 21 healthy volunteers matched to the patients for age, sex and body mass index (eight men, 13 women, 51.6 +/- 9.3 years old). Insulin values were related to the rate-pressure product increase at first exercise stage. The glucose values as well as the insulin values during fasting were similar in syndrome X patients and in controls. However, significantly higher insulin values (mU/l) were observed at 60 (P < 0.01) and 120 min (P < 0.005) in syndrome X patients (median 75.5 and 52, range 43-290 and 6.1-212, respectively) than in controls (median 47.5 and 24.5, range 8-195.6 and 5.2-164, respectively). A considerable overlap of insulin values, however, was observed between the two groups, with abnormal values even during fasting. For a specificity of 95%, an abnormal insulin value had a sensitivity of between 19 and 24% and a diagnostic accuracy of 57-60%. A significant positive correlation was found between insulin levels after the glucose load and the rate-pressure product increment with exercise (60 min, r = 0.60; 120 min, r = 0.65). Hyperinsulinaemia may be pathogenetically involved in syndrome X patients, in close relation to the higher sympathetic drive that characterizes this syndrome. However, the wide range of insulin values, frequently overlapping with normal values, limits the usefulness of this abnormality as a marker of the syndrome.

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

This study was designed to assess the clinical, hemodynamic and diagnostic effects of the addition of dobutamine to dipyridamole echocardiography. 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). 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. 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). 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.