Role of echocardiography in the assessment of left ventricular thrombus embolic potential after anterior acute myocardial infarction.

The contribution of cardiac ultrasound in assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction was verified in a prospective study of serial echocardiograms (mean, 18.9 examinations per patient) obtained over a long-term period (1-72 months; mean, 38±12). The study population comprised 222 patients (162 men; age, 64±11 years) with a first anterior acute myocardial infarction, treated with thrombolysis (group A) or receiving no antithrombolic therapy (group B). Embolism occurred in a total of 12 patients (11 with a left ventricular thrombus; p<0.005) and was more frequent in group B (10 patients; p<0.04). Predictors of embolism were the absence of thrombolysis, detection of a left ventricular thrombus, protrusion or mobility of the thrombus, and morphologic changes in the thrombus over time. Patients in group A had a lower incidence of each of these predictors, and a higher thrombus resolution rate. An appropriate echocardiographic protocol is crucial to assessment of the embolic potential of left ventricular thrombi after anterior acute myocardial infarction and may help to identify candidates for aggressive antithrombotic therapy (c)2001 CHF, Inc.

Use of a common computerized program for echocardiogram archiving and reporting over a regional territory: feasibility and clinical and research impact during a 5-year experience.

The aims of this study were to optimize interlaboratory standardization of echocardiographic reporting (qualitative terms and quantitative parameters) and to evaluate the feasibility and clinical and research impact of collecting echocardiographic data in a standard computerized format over a geographical territory. In April 1992, a computer program of echocardiogram archiving and reporting (ARCE) was distributed at no cost to the 23 hospital echocardiographic laboratories operating in our region (Liguria). In April 1993 (1-year survey), 16 (70%) of the 23 hospital echo laboratories operating in our region were routinely using ARCE. In April 1997 (4-year survey ), 21 (87%) of the 24 echo laboratories were routinely using the system and 128,642 echocardiograms had been databased. ARCE is a powerful tool both for education and training in cardiac ultrasound and for undertaking multicenter studies by 95% of the users. Regarding the quality improvement process, we achieved 3 main goals: (1) a unique report format from 87% of Ligurian echo laboratories, which improved the communication between echocardiographers and other physicians; (2) development of specific, Ligurian population-based reference limits for M-mode and 2-dimensional quantitative parameters; and (3) interlaboratory comparison and standardization of both quantitative and semiquantitative evaluation of heart valve disease, left ventricular systolic and diastolic function, valve prosthesis function, and left ventricular hypertrophy. Regarding the scientific activity in Liguria, 9 multicenter studies in which 15 Ligurian echo laboratories took part were organized and completed in 5 years. Our 5-year experience shows that it is possible to create a large database of echocardiographic data that uses a fast, easy-access, and easy-to-use program of echo archiving and reporting that contains standardized variables. The use of this program on a regional territory scale appeared feasible and useful both for educational and training purposes. In addition, it stimulated the quality improvement process in echocardiography as well as performance of epidemiologic and clinical multicenter studies.

Long-term prospective assessment of left ventricular thrombus in anterior wall acute myocardial infarction and implications for a rational approach to embolic risk.

To prospectively assess the predictive value of left ventricular (LV) thrombus anatomy for defining the embolic risk after acute myocardial infarction (AMI), 2 comparable groups of patients with a first anterior AMI (group A, 97 thrombolysed patients; group B, 125 patients untreated with antithrombotic drugs [total 222]) underwent prospective serial echocardiography (follow-up 39 +/- 13 months) at different time periods. LV thrombi were detected in 26 patients in group A (27%) and in 71 in group B (57%; p <0.005). Embolism occurred in 12 patients (5.4%; 1 in group A [1%] vs 11% in group B [9%], p < 0.04). At multivariate analysis, thrombus morphologic changes were the most powerful predictor of embolism (p <0.001), followed by protruding shape (p <0.01) and mobility (p <0.02). In patients untreated with thrombolysis, a higher occurrence of thrombus morphologic changes (48% vs 8%, p <0.002) and protruding shape (69% vs 31%, p <0.002) were observed, whereas thrombus mobility was similar in the 2 groups (18% vs 8%, p = NS). Thrombus resolution occurred more frequently in thrombolysed patients (85% vs 56%, p <0.002). Thus, after anterior AMI, changes in LV thrombus anatomy frequently occur and appear the most powerful predictor of embolization. A minor prevalence of thrombus, a more favorable thrombus anatomy, and a higher resolution rate may contribute to reduce embolic risk after thrombolysis.

Predischarge two-dimensional echocardiographic evaluation of left ventricular thrombosis after acute myocardial infarction in the GISSI-3 study.

Left ventricular (LV) thrombosis can be found in patients with acute myocardial infarction (AMI). No wide multicenter trial on AMI has provided information about LV thrombosis until now. The protocol of the GISSI-3 study included the search for the presence of LV thrombosis in patients from 200 coronary care units that did not specifically focus on LV thrombosis. We examined the GISSI-3 database results related to 8,326 patients at low to medium risk for LV thrombi in which a predischarge echocardiogram (9 +/- 5 days) was available. LV thrombosis was found in 427 patients (5.1%): 292 of 2,544 patients (11.5%) with anterior AMI and in 135 of 5,782 patients (2.3%) with AMI in other sites (p <0.0001). The incidence of LV thrombosis was higher in patients with ejection fraction < or = 40% (151 of 1,432 [10.5%] vs 276 of 6,894 [4%]; p <0.0001) both in the total population and in the subgroup with anterior AMI (106 of 597 [17.8%] vs 186 of 1,947 [9.6%]; p <0.0001). Multivariate analysis showed that only the Killip class > I and early intravenous beta-blocker administration were independently associated with higher LV thrombosis risk in the subgroup of patients with anterior AMI (odds ratio 1.75, 95% confidence interval 1.28 to 2.39; odds ratio 1.32, 95% confidence interval 1.02 to 1.72, respectively). In patients with anterior AMI, oral beta-blocker therapy given or not given after early intravenous beta-blocker administration does not influence the occurrence of LV thrombosis. The rate of LV thrombosis was similar in patients treated or not treated with nitrates and lisinopril both in the total population and in patients with anterior and nonanterior AMI. In conclusion, in the GISSI-3 population at low to medium risk for LV thrombi, the highest rate of occurrence of LV thrombosis was found among patients with anterior AMI and an ejection fraction < 40%. Killip class > I and the early intravenous beta-blocker administration were the only variables independently associated with a higher predischarge incidence of LV thrombosis after anterior AMI.

Chronic aneurysmatic dilatation: a possible source of lethal embolization in patients with acute myocardial infarction undergoing thrombolysis.

Left ventricular thrombosis is relatively common after acute myocardial infarction, especially in the anterior site, and represents a possible cause of potentially lethal peripheral embolization 1. Therefore, several studies have been performed in order to assess the efficacy of different antithrombotic drugs in resolving the detected thrombi or reducing their embolic potential. Fibrinolytic agents appear effective in this regard: in the majority of cases, they produce complete lysis and resolution of the thrombi. However, this treatment may itself cause embolic complications by producing a rapid fragmentation of thrombus and the subsequent emission of disrupted portions of the intracardiac mass into the systemic vascular bed [2]. This dramatic effect of thrombolysis has suggested the possibility that even the standard treatment of acute myocardial infarction with fibrinolysis implies a danger of embolization in those patients in whom a left ventricular thrombus may be present either from a previous myocardial infarction or from a very early thrombus development. However, this hypothesis has not yet been confirmed by direct observation. We report the case of a patient with a first acute anterior myocardial infarction, in whom the thrombolytic treatment induced lysis and embolization from a left ventricular thrombus present in an aneurysmatic dilatation of the infero-posterior wall due to a previous inferior myocardial infarction.

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

In recent years, increasing evidence has pointed to the potential of dipyridamole stress echocardiography as a fast, effective, inexpensive method of risk stratification after an acute myocardial infarction. A very early stratification by this test could improve the patient's management and reduce the duration of in-hospital stay, and, thus, the costs. Two-hundred and fifty-one consecutive patients (208 male, age 58 +/- 11) with a two-dimensional echocardiogram of good technical quality underwent a dipyridamole echocardiographic test (DET) 70 +/- 6 h after an acute myocardial infarction. Criterion for positivity was the identification of a transient regional asynergy that was absent or of a lower degree in the baseline examination. Positivity was defined as 'at low-dose' or 'at high-dose' if the asynergy was detected before or after the 8th min of a drug infusion. All tests were performed without any major side effects. DET was positive in 149 (59%) and negative in 102 (41%) patients. During the hospital stay, cardiac events (death, reinfarction, angina) occurred in 52/251 patients: in 49/149 with a positive and in 3/102 with a negative test (sensitivity 94%, negative predictive value 97%, P < 0.00001). Severe events (death and reinfarction) occurred in 14/251: in 12/149 with a positive DET and in 2/102 with a negative DET (sensitivity 86%; negative predictive value: 98%; P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular thrombus in anterior acute myocardial infarction after thrombolysis. A GISSI-2 connected study.

BACKGROUND: Streptokinase reduces the incidence of left ventricular thrombosis after acute myocardial infarction. However, it is unknown whether a similar effect can be obtained with different thrombolytic agents and whether subcutaneous calcium heparin can have an additional efficacy. METHODS AND RESULTS: To compare the effects of two different thrombolytic agents combined or not with heparin on the incidence and features of left ventricular thrombi and their related embolic events, we performed a GISSI-2 ancillary echocardiographic study (the first echocardiogram obtained within 48 hours of symptoms onset and the second before hospital discharge) that enrolled 180 consecutive patients (mean age, 63 +/- 11 years, 142 men) with a first anterior acute myocardial infarction. Patients were randomized into four groups of treatment: recombinant tissue-type plasminogen activator (rt-PA) (n = 47), rt-PA plus heparin (n = 45), streptokinase (n = 39), and streptokinase plus heparin (n = 49). Left ventricular thrombosis was observed in 51 of 180 patients (28%). No significant differences were found concerning the incidence of thrombi in the four treatment groups. Mural shape of left ventricular thrombi was found more frequently than the protruding shape (71% versus 29% at the first examination, 64% versus 36% at the second), particularly in heparin-treated patients (93% versus 7% at first examination, 70% versus 30% at the second). Only one embolic event (0.5%) occurred during the hospitalization. CONCLUSIONS: We conclude that 1) the rate of left ventricular thrombi does not differ in patients with acute myocardial infarction treated either with streptokinase or rt-PA, 2) subcutaneous heparin, when begun 12 hours after intravenous thrombolysis, does not appear to further reduce the occurrence of thrombi but seems to influence the shape of left ventricular thrombi, and 3) during the predischarge period, embolic events are rare in patients treated by thrombolysis.

Early appearance of left ventricular thrombi after anterior myocardial infarction: a marker of higher in-hospital mortality in patients not treated with antithrombotic drugs.

Left ventricular thrombus may develop both early and late after acute anterior myocardial infarction. To assess the possible prognostic implication of the time of thrombus appearance, 125 patients (87 males; age ranging from 35 to 92 years, mean: 65 +/- 10 years) consecutively admitted to our coronary care unit within 24 h of a first acute anterior myocardial infarction, untreated with antithrombotic drugs, underwent serial two-dimensional echocardiographic studies during hospitalization, then monthly for a follow-up of 1-48 (mean: 23 +/- 16) months among survivors. Left ventricular thrombi, detected in 71 patients (57%), appeared from 1 to 362 (mean: 13 +/- 44) days after acute infarction. In 40 patients (56%), early thrombus development, within 48 h of symptom onset, was noted. During the study period, 52 patients (42%) died. Global mortality rate was similar in patients with thrombi compared with those without thrombi (32/71: 45%, vs 20/54: 37%; P = ns). However, in-hospital mortality of patients who developed left ventricular thrombi within 48 h (17/40: 42.5%) was significantly higher compared with both patients with later thrombus appearance (4/31: 13%; P less than 0.008) and those without thrombi (10/54: 20%; P less than 0.01). Embolic events were more frequent in patients with thrombi (9/71, 13% vs 1/54, 2%; P less than 0.02), but there was no relationship with the time of thrombus appearance. The values of peak CPK levels and the degree of left ventricular wall motion abnormalities observed in patients with early left ventricular thrombus were significantly higher than the values detected in patients without thrombi, but similar to those obtained in patients with later thrombus occurrence.(ABSTRACT TRUNCATED AT 250 WORDS)

Left ventricular thrombi: changes in size and in platelet deposition during treatment with indobufen and ticlopidine.

This study was designed to evaluate whether indobufen and ticlopidine can induce changes in the size of left ventricular thrombi and variations in the deposition of platelets on thrombus surface. Forty-seven patients with left ventricular thrombosis, who were not treated with antithrombotic drugs, were prospectively evaluated with 111In-oxine platelet imaging and two-dimensional echocardiography. The first scintigraphic examination was negative in 15 of the 47 patients with left ventricular thrombosis, thus they were excluded from further evaluation. The remaining 32 patients with evidence of labeled platelet deposition on the thrombus were divided into three groups. Group 1 comprises 11 patients treated with different doses of ticlopidine: 6 with 250 mg/day, and 5 with 500 mg/day. Group 2 comprises 12 patients who received 400 mg/day of indobufen. Group 3 comprises 9 patients who were not treated with antithrombotic drugs. All 32 patients underwent repeated 111In-oxine platelet imaging and echocardiography 40 +/- 11 days after the first examination. During treatment with ticlopidine, deposition of labeled platelets on the thrombus became absent in 2 patients (500 mg/day), and reduced in 5 (2 treated with 250 and 3 with 500 mg/day). A decrease of platelet deposition on the thrombus was also observed in 5 of the 12 patients receiving indobufen and in only 1 of 9 controls. With regard to thrombus dimensions, 1 patient treated with ticlopidine showed a decrease in thrombus size associated with a reduction of the scintigraphic activity. In conclusion, a decrease of the platelet uptake on the thrombus surface, without significant changes in the size, was detected in most patients during treatment with indobufen and ticlopidine.(ABSTRACT TRUNCATED AT 250 WORDS)

Severity of arrhythmias and extent of hypertrophy in hypertrophic cardiomyopathy.

To evaluate the relationship between the extent of left ventricular hypertrophy and ventricular or atrial arrhythmias, 77 patients with hypertrophic cardiomyopathy underwent two-dimensional echocardiography and 24-hour Holter monitoring. Antiarrhythmic treatment was discontinued before the study. Hypertrophy was septal in 33 patients, "extensive" (i.e., involving the septum and free wall) in 38 patients, and predominantly apical in six patients. Lown grade I and II ventricular arrhythmias were detected in 37% of patients, grade III in 21%, and grade IV in 29%. Atrial extrasystoles were seen in 52% of patients and chronic atrial fibrillation in 13%. More serious ventricular arrhythmias (Lown grades III and IV) occurred significantly more frequently in patients with extensive than in those with only septal hypertrophy (22/38 vs 11/33; p less than 0.001); similarly, chronic atrial fibrillation occurred more commonly in those with extensive hypertrophy (9/38 vs 1/33; p less than 0.01). During a mean follow-up period of 2.6 years, three patients died. All had a pattern of extensive hypertrophy. Two of them had ventricular tachycardia and the third had chronic atrial fibrillation. Results of this study suggest that an echocardiographic finding of extensive hypertrophy represents a useful marker for detecting patients at increased risk for serious ventricular and atrial arrhythmias.

Influence of thrombolytic treatment followed by full dose anticoagulation on the frequency of left ventricular thrombi in acute myocardial infarction.

This study evaluated the influence of thrombolysis followed by full anticoagulation on the frequency of left ventricular (LV) thrombi after acute myocardial infarction (AMI). Nineteen consecutive patients with a first anterior wall AMI who received 1,500,000 IU of streptokinase within 3 hours of symptom onset, followed by full anticoagulation, underwent echocardiographic studies within 24 hours of symptoms, and then on days 2, 3, 5, 7, 12, 30 and 90. Forty-four patients, with comparable clinical features and echocardiographic protocol but without antithrombotic therapy, served as the control group. LV thrombi developed in 4 of 19 (21%) treated patients and in 23 of 44 (52%) control subjects (p = 0.02). LV aneurysm or major wall motion abnormalities were noted in 8 of 19 (42%) treated patients and in 30 of 44 (68%) control subjects (p less than 0.05). No significant difference was found between treated and untreated patients when comparing the incidence of thrombi in the subgroups of patients with aneurysm or major wall motion abnormalities (3 of 8 vs 21 of 30) and in the subgroups with less extensive LV dysfunction. Thrombi disappeared during hospitalization in 3 of 4 treated patients, but in none of the controls. Fewer patients treated with intravenous streptokinase followed by full anticoagulation developed LV thrombi compared to patients treated with conventional therapy. This difference may be related to a reduced occurrence of major LV wall motion abnormalities. Resolution of thrombi frequently occurs in the hospital phase of AMI; therefore, only frequent echocardiographic examinations can assess the true frequency of LV thrombi.

[Supravalvular aortic stenosis: clinical and genetic study of a family group]. / Stenosi aortica sopravalvolare: studio clinico e genetico di un'ampia famiglia.

We describe a family with a high frequency of supravalvular aortic stenosis. The family includes 5 generations and 80 subjects (prospective study in 66, on whom physical examination, ECG, M-mode and two-dimensional echocardiogram were performed, and retrospective analysis of available data in 14). This is the largest family group with this disease studied so far. Thirty-six subjects (45%) were found to be affected. On the basis of the echocardiographic image and of the haemodynamic gradient (when available), three different degrees of supravalvular aortic stenosis were identified. The disease was found to be severe in 8 subjects (22%), moderate in 6 (17%), mild in 13 (36%) and undefined in 8 (22%). In 4 cases multiple pulmonary stenoses were associated with supravalvular aortic stenosis, while in one subject multiple pulmonary stenoses were noted in the absence of aortic abnormalities. In the family we studied, the supravalvular aortic stenosis gene is transmitted with a pattern of inheritance consistent with an autosomal dominant trait with variable expressivity and penetrance (penetrance coefficient = 0.86). A high mortality rate in early childhood was observed, while symptoms and ECG abnormalities were not related to the degree of the stenosis. Furthermore, we found a high rate of mitral valve echocardiographic abnormalities, such as mitral prolapse and systolic anterior motion. The absence of Williams dysmorphic somatic features in the many generations as well as in the large number of patients we studied, appears to exclude the coexistence of Williams and Eisenberg's syndromes in the same family group.

Familial supravalvular aortic stenosis: a genetic study.

Supravalvular aortic stenosis (McKusick 18550) is a rare hereditary condition with autosomal dominant transmission. However, the available data have been limited to small family groups which do not allow the definition of the degree of penetrance of the disease. The present study describes a large family with a high frequency of supravalvular aortic stenosis including five generations and 80 subjects, the largest family group with this disease studied so far. The study was carried out prospectively in 66 subjects (clinical examination, ECG, M mode and two dimensional echocardiography). In 14 subjects available data were examined retrospectively. In 10 patients cardiac catheterisation was performed (prospective study in eight). The disease was present in 36 (45%) of the 80 subjects investigated, on the basis of clinical, echocardiographic, and haemodynamic (when available) criteria. The disease was found to be severe in eight cases (22%), moderate in six cases (17%), mild in 13 (36%), and undefined in eight (22%) patients. In one case (3%), multiple pulmonary stenoses were noted in the absence of supravalvular aortic stenosis. Genetic analysis of these data shows, for the first time, the degree of penetrance of the supravalvular aortic stenosis trait (K = 0.86) and confirms that it is transmitted with incomplete penetrance and variable expressivity.

Activity of left ventricular thrombi of different ages. Assessment with indium-oxine platelet imaging and cross-sectional echocardiography.

To evaluate the possible relation between the age of intracardiac thrombi and the presence and degree of their activity, 29 patients with left ventricular thrombi that developed after an anterior myocardial infarction were evaluated by means of 111In-oxine autologous platelet imaging. None of the patients was treated with anticoagulants or platelet inhibitors during either the acute phase of infarction or the follow-up. The time of appearance and the shape of left ventricular thrombi were assessed by serial cross-sectional echocardiograms, obtained within 24 hours of onset of the chest pain, every 24 hours until the fifth day, every 48 hours until the 15th day, and then every month for a follow-up of 1 to 17 months (mean: 8 months). At the time of the scintigraphic examination, left ventricular thrombi were aged 1 month in 9 patients, and 2 to 14 months in the remaining 20 patients. 111In-oxine imaging with autologous platelets was obtained in all patients at 4, 24, 48 and 72 hours, in the sagittal, 30 degrees and 45 degrees left anterior oblique projections. In 25 patients the degree of haematological activity of the thrombi was evaluated by dividing the values of thrombus activity/background activity, obtained at 4, 24, 48 and 72 hours, respectively, by the value observed at 4 hours (uptake index). Scintigraphic imaging showed the presence of an active thrombus in every patient. In the 9 patients with recent thrombi, the uptake index was significantly greater than in subjects with older ones (P less than 0.01). Hence, in patients with anterior myocardial infarction, untreated with anticoagulants or platelet inhibitors, haematologically active thrombi can be observed even more than one year after their appearance. The uptake of platelets on the surface of thrombi is greater in recent left ventricular thrombi than in older ones.

Spontaneous morphologic changes in left ventricular thrombi: a prospective two-dimensional echocardiographic study.

Previous retrospective echocardiographic studies have reported a higher embolic potential of left ventricular thrombi with protruding configuration and patterns of mobility. The present study was performed to prospectively assess the shape and mobility patterns of left ventricular thrombi and their spontaneous changes with time. Two-dimensional echocardiograms were obtained in 109 consecutive patients with acute anterior myocardial infarction within 24 hr of the onset of symptoms, every 24 hr until day 5, every 48 hr until day 15, and then every month for a follow-up of 1 to 29 (mean 14 +/- 8) months in the survivors. None of the patients were treated with anticoagulants or platelet inhibitors during the study period. Left ventricular thrombi, detected in 59 patients (54%), appeared from 1 to 362 (mean 12 +/- 47) days after myocardial infarction. At first detection, the shape was mural in 21 patients and protruding in 38; patterns of mobility were present in eight patients. During follow-up, changes in the shape of the thrombi were noted in 24 patients (41%; from mural to protruding in nine, from protruding to mural in 15). These variations were encountered between 2 and 490 (mean 64 +/- 117) days after the first observation of the thrombus. Patterns of mobility, previously detected in eight patients, disappeared in five of eight within 2 to 28 (mean 14 +/- 11) days.(ABSTRACT TRUNCATED AT 250 WORDS)

[Echocardiographic and anatomic evaluation of left ventricular thrombosis]. / Valutazione ecocardiografica ed anatomica della trombosi ventricolare sinistra.

The aim of this study was to assess the correspondence between two-dimensional echocardiographic (2D-Echo) and anatomic features of left ventricular thrombi (LVT), with particular reference to LVT shape and dimensions. The study population was composed of 23 patients who were admitted to our intensive cardiac care unit with an anterior acute myocardial infarction and who died during the hospitalization. Every patient underwent serial echocardiographic examinations, the last one performed within the 24 hours preceding death. The diagnosis of LVT required the agreement of three independent observers. Doubtful cases were considered as negative. With regard to shape, the LVT were defined as mural or protruding. Two measures of the LVT were obtained in each case: the longest dimension and the greatest one perpendicular to the initial dimension. At post-mortem examination we obtained sections of the heart comparable with an echocardiographic four chamber view. LVT were detected by 2D-Echo in 12/23 cases. Post-mortem examination confirmed the presence of LVT in these 12 patients. A thin apical thrombotic layer, whose presence had been defined previously as doubtful, was observed in another patient. The sensitivity of 2D-Echo was 92% and the specificity 100%. At 2D-Echo, shape was mural in 2 patients and protruding in 10. Complete agreement was found between 2D-Echo and anatomic findings as far as the morphology of LVT is concerned. The 2D-Echo measurements of LVT showed a high correlation with autopsy (r = 0.95; r = 0.86); we conclude that 2D-Echo provides accurate evaluations of the shape and the dimensions of LVT.

[Normal behavior during the exercise test of the left ventricular ejection fraction determined by an angioscintigraphic method]. / Sul comportamento normale durante sforzo della frazione di eiezione ventricolare sinistra determinata con metodo angioscintigrafico.

UNLABELLED: The correct definition of left ventricular ejection fraction (LVEF) normal response to exercise is still debated. The lack of unanimous agreement firstly depends on the different normality criteria adopted in literature. In order to make ligh, we carefully reviewed several papers on this matter, and performed exercise radionuclide angiography (RNA), by multiple gated blood pool, in 2 different populations. I group: 39 normal subjects, selected on the basis of normal clinical examinations, ECG, X-ray film, exercise test, at rest LVEF greater than 50%: 20 males, mean age 43 +/- 13%. II group: 22 patients, abnormal from the clinical point of view, but elsewhere included in control groups: 13 males, mean age 54 +/- 9%. 14 of them refer only atypical chest pain, in 5 the sole abnormal finding is an exercise-induced ST depression greater than 1 mm, in 2 a left bundle branch block at rest, 1 patient suffers from X syndrome. Symptom limited exercise RNA was carried out by adopting a semi supine (40 degrees) cycloergometer, with a 25 watt initial workload and 25 watt subsequent increases every 3 minutes; count acquisition lasted 2 minutes, from the end of the 1st to the end of the 3rd, during each stage of the test. RESULTS: I group: constant LVEF increment during exercise in all subjects: mean LVEF at rest was 65 +/- 8%, at maximum workload 80 +/- 8%: mean increase was 15 +/- 7%.(ABSTRACT TRUNCATED AT 250 WORDS)