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SUMMARYObjective — This study explored the effectiveness of a psychoeducational family intervention for schizophrenia on patients' clinical status and disability and relatives' burden and perceived support. Methods — The study has been carried out in 17 mental health centres. In each of them, 2 professionals were trained in a psychoeducational intervention and applied it for six months with families of users with schizophrenia. At baseline and six months later, patients' clinical status and disability, and relatives' burden, social network and professional support were assessed by validated tools. Results — Of the seventy-one recruited families, 48 (68%) completed the intervention. At six months, a significant improvement was found in patients' clinical status and social functioning, as well as in relatives' burden and social and professional support. In particular, the percentage of patients with poor or very poor global social functioning dropped from 50% to 27% at six months. Forty percent of patients and 45% of relatives reported a significant improvement in their social contacts over the intervention period. Conclusions — The results of this study confirm the hypothesis that psychoeducational family interventions may have a significant effect on social outcome and family burden in schizophrenia when provided in routine conditions.Declaration of Interest: none of the authors has had any interest or he/she has received any form of support, including that from drug companies and honoraria for lectures and consultancies, potentially in conflict with this scientific work. None of the authors has received any form of fee for his/her participation in this study. This study was supported by grants received from the “M. Lugli” Foundation (grant n. 2/18/8) and from the National Institute of Health, Italy (grant no. 1AL/F3).

SUMMARYAims – This study aims to explore: a) the feasibility of psycho-educational interventions for families of users with schizophrenia in clinical practice by trained staff; b) the benefits and problems encountered by professionals in the use of these interventions. Methods – 46 professionals from 23 Italian Mental Health Sen'ices (MHS) attended at a three-module training course in psycho-educational interventions and four supervisions in the subsequent year. Following the course, participants provided the intervention to families of users with schizophrenia. The difficulties and benefits encountered by trainees to use the intervention were registered on the Family Intervention Schedule.Results – 83% of the participants completed the training course. Following the course, the intervention started in 71 families from 17 MHS. 76% of trainees provided the intervention to 2-5 families, while 13% of them only held informative sessions on schizophrenia. During the supervision period, the organisational difficulties experienced by the professionals were stable, while the benefits increased. Differences in benefits and difficulties were detected in relation to the trainees’ experience and professional roles. Conclusions – It is possible to introduce psycho-educational interventions in MHS after a relatively brief period of training and supervision of the staff. Organisational difficulties need to be addressed to increase the dissemination of these interventions on a large scale.Declaration of Interest: None of the authors has had any interest or he/she has received any form of support, including that from drug companies and honoraria for lectures and consultancies, potentially in conflict with this scientific work. None of the authors has received any form of fee for his/her participation in this study. This study was supported by grants received from the “M. Lugli” Foundation (grant n. 2/18/8) and from the National Institute of Health, Italy (grant no. 1AL/F3).

Objectives. This study was designed to compare exercise, dipyridamole and dobutamine echocardiography in the same patients and to evaluate, by measuring physiologic and echocardiographic variables, the mechanisms by which exercise and dobutamine induce ischemia. Background. The diagnostic value of stress echocardiography has been widely reported, but the specific effects of exercise, dipyridamole and dobutamine have not been directly compared. Furthermore, no echocardiographic study has evaluated left ventricular volume changes at ischemic threshold during exercise and dobutamine administration. Methods. One hundred patients with suspected (Group A, n = 60) or known (Group B, n = 40) coronary artery disease underwent all three tests in random order. Results. In Group A, the sensitivities of exercise (mean 76%, 95% confidence interval [CI] 58% to 94%) and of dobutamine echocardiography (72%, 95% CI 53% to 91%) were higher than that of dipyridamole (52%, 95% Cl 31% to 73%; p = 0.01 and p = 0.02, respectively). Specificity did not differ significantly among tests (94% for exercise [95% CI 86% to 100%] and 97% for dipyridamole and dobutamine [95% CI 91% to 100%]). Accuracy was identical for exercise and dobutamine (87%) and higher than that for dipyridamole (78%, p = 0.06). In Group B, the accuracy in predicting coronary disease extent was 71% for exercise, 33% for dipyridamole and 75% for dobutamine. At ischemic threshold, end-systolic volume index and the ratio of systolic blood pressure to end-systolic volume, a variable related to myocardial contractility, were significantly lower and higher, respectively, with dobutamine than during exercise (p Conclusions. In a clinical setting, exercise echocardiography should represent the first diagnostic approach because it has high diagnostic efficacy and provides additional information on exercise capacity; pharmacologic stress, particularly that of dobutamine, provides a pivotal diagnostic tool when exercise is not feasible or its results are nondiagnostic. Our preliminary data on echocardiographic evaluation at ischemic threshold support the view that myocardial contractility is a major factor in inducing ischemia during dobutamine infusion.

Although exercise stress echocardiography is currently used to evaluate coronary artery disease (CAD) patients, the best exercise methodology is still undefined. The objectives of the study were: (1) to compare supine bicycle stress echocardiography (SBSE) and treadmill in the evaluation of CAD; and (2) to define, in normal subjects, the different behavior of factors determining MVO 2 with treadmill and SBSE. We selected 10 male patients with CAD (group A), and 10 male control subjects (group B). Each patient underwent SBSE and treadmill testing in random order. We studied heart rate, systolic blood pressure, heart rate × systolic blood pressure, and end-diastolic and end-systolic volume indexes. In group A, we also studied wall motion score index (according to the American Society of Echocardiography) and in group B, systolic blood pressure/end-systolic volume index. The results were as follows: Group A : SBSE resulted in significantly lower work load, heart rate, and significantly higher systolic blood pressure, heart rate × systolic blood pressure, end-diastolic volume index, end-systolic volume index, and wall motion score index. SBSE showed wall motion abnormalities in each patient, whereas treadmill did not detect wall motion abnormalities in 4 patients (3 single-vessel; 1 multivessel); of the other 6 patients, 2 showed a lower wall motion score index and 4 did not show any difference in left ventricle kinetics with the 2 methodologies of exercise. Mean acquisition time for postexercise images was 72 ± 6 seconds. Group B : SBSE resulted in lower work load, heart rate, heart rate × systolic blood pressure, systolic blood pressure/end-systolic volume index, and higher end-diastolic volume index and end-systolic volume index. Systolic blood pressure was similar with SBSE and treadmill testing. In conclusion, our experience suggests SBSE is a highly accurate diagnostic tool for evaluating CAD compared with treadmill testing; the maximum cardiovascular performance can be achieved with lower values of heart rate, suggesting the echo test is more feasible. Treadmill testing could lose important information about the existence, extension, and location of CAD; in contrast, SBSE detects even small, quickly reversible wall motion abnormalities.

Background: Color kinesis (CK) is a recently developed echocardiographic technique based on acoustic quantification that automatically tracks and displays endocardial motion in real time and has been used in initial studies to improve the evaluation of global and regional wall motion. Hypothesis: For further validation of the use of CK for analysis of segmental ventricular dysfunction, we assessed its sensitivity and specificity for detection of regional systolic and diastolic wall motion abnormalities in patients with coronary artery disease (CAD). Methods: Two-dimensional (2-D) echocardiography and CK were used to study 15 normal subjects and 63 patients with technically good quality echocardiographic tracings, who underwent coronary arteriography within 1 month of echocardiography. Significant (>70% luminal diameter stenosis) CAD was present in 50 patients (79%). Results: Color kinesis tracked endocardial motion accurately in 93% of left ventricular segments. Wall motion score, systolic segmental endocardial motion (SEM), and the time of systolic SEM (tSEM) and diastolic (tDEM) segmental endocardial motion were calculated. Intra- and interobserver variability were within narrow limits. SEM and tSEM were significantly lower and tDEM was significantly higher in the patient population than in the control group (p< 0.001). Comparison between CK and 2-D echocardiography showed a correlation coefficient of 0.81 between the two techniques. The score was identically graded in 74% of segments, with concordance of 82% in diagnosing segments as abnormal. Interobserver concordance was 86% for CK (r=0.85) and 81% for 2-D echocardiography (r=0.80). The sensitivity and specificity of systolic and diastolic CK parameters for the detection of CAD were 88 and 92% and 77 and 85%, respectively. The positive predictive values were 93 and 96%, respectively, the negative predictive values were 63 and 73%, respectively, and the overall accuracy was 86 and 91%, respectively. Conclusions: Our data suggest that CK is a feasible and sensitive technique for identifying regional systolic as well as diastolic wall motion abnormalities in patients with CAD.

In order to determine whether the diastolic rate of ventricular volume change obtained on-line with an automatic border detection (ABD) system during dobutamine stress echocardiography (DSE) would provide an interpretation of the diastolic ventricular response to the drug in quantitative terms in the assessment of coronary artery disease, we studied, with ABD and DSE, 59 patients who underwent coronary arteriography within 2 months of the stress test. Eleven patients had normal coronary findings or non-significant coronary lesions. Significant (or =70% diameter stenosis) coronary artery disease (CAD) was present in 48 patients (81%). Dobutamine stress echocardiography (DSE) to a maximal dose of 50 microg/kg per min was performed in all patients. ABD images were acquired at rest and at the peak of infusion along with conventional two-dimensional images. The following measurements were evaluated: left ventricular end-diastolic volume (LVEDV), left ventricular end-systolic volume (LVESV), left ventricular ejection fraction (LVEF), slope of rapid filling segment (RFS), peak filling rate (PFR), rapid filling phase fractional change (RFFC). Patients with non-significant coronary artery lesions exhibited a hyperdynamic response with an LVEF increment of at least 20% from baseline to peak drug infusion. In these patients the effect of dobutamine produced an increase of RFS from 35.5+/-5.6 to 86.5+/-10.5 ml/s, an increase of PFR from 4.4+/-0.6 to 6.8+/-0.6 EDV/s, and an increase of RFFC from 74+/-8 to 92+/-5% (P0.001). Of the 48 patients with coronary artery disease, 27 had20% LVEF increase at peak dobutamine infusion. Four of 22 patients with single vessel disease and 23 of 26 patients with multivessel disease had an abnormal systolic response. After dobutamine infusion single vessel CAD patients showed a decrease of RFS from 33.4+/-5.3 to 26.7+/-5.9 ml/s, a decrease of PFR from 3.8+/-0.7 to 3.0+/-0.7 EDV/s, and a decrease of RFFC from 73+/-6 to 59+/-4% (P0.001). Multivessel CAD patients showed a decrease of RFS from 32.0+/-5.9 to 23.1+/-4.1 ml/s, a decrease of PFR form 3.8+/-0.6 to 2.8+/-0.6 EDV/s, and a decrease of RFFC from 71+/-5 to 54+/-8% (P0.001). The overall sensitivity of detecting CAD was 85% for conventional DSE and 90% for ABD-DSE (P=NS). The sensitivities of detecting patients with single vessel and multivessel CAD with conventional DSE were 68 and 92%, respectively, and with ABD-DSE were 91% (P0.01) and 96% (P=NS), respectively. Our results show that an abnormal diastolic as well as systolic response during on-line quantitative assessment of dobutamine stress echocardiography is a sensitive marker of coronary artery disease and is predictive for the detection of extensive lesions. The described measurements can be utilized to improve the DSE sensitivity in identifying coronary artery disease. On-line quantitation of diastolic indexes with ABD can represent another step toward obtaining uniform results after stress echocardiography.

Nineteen patients (16 men and 3 women, mean age 51 years) with previous anterior myocardial infarction and severe stenosis (> or = 90%) of the left anterior descending coronary artery were studied by magnetic resonance imaging (MRI) without and with contrast media to verify the capability of MRI in identifying viable myocardium in areas of severe systolic dysfunction. In corresponding left ventricular segments, a comparison was made between regional signal intensities (SI) determined on MRI images before and 4, 8, 12, and 30 minutes after administration of paramagnetic contrast media (gadolinium diethylenetriaminepentaacetic acid, 0.4 mmol/kg intravenously) and metabolic parameters determined by iodine 123 phenylpentadecanoic acid (IPPA) scintigraphy. The SI and the time of maximum postcontrast enhancement were analyzed by dividing the left ventricle into 11 segments. Each segment was classified as normal (group 1, n = 116), hibernating (group 2, n = 50), or necrotic (group 3, n = 43) on the basis of the IPPA washout rate (> 30%, 10% to 30%, and < 10%, respectively). Regional SI demonstrated significant differences in absolute values at 12 minutes (group 3: 1.62 +/- 0.58 vs group 1: 1.32 +/- 0.52, p < 0.01, and vs group 2: 1.34 +/- 0.48, p < 0.05) and at 30 minutes (group 3: 1.71 +/- 0.47 vs group 1: 1.21 +/- 0.55, p < 0.01, and vs group 2: 1.49 +/- 0.57, p < 0.05) and in temporal distribution. These results suggest that MRI has a potential role in differentiating viable from necrotic myocardium in patients with chronic severe systolic dysfunction.

The aim of this study was to examine whether myocardial contrast echocardiography (MCE) may be used to study regional myocardial blood flow distribution during dipyriamole-induced hyperemia. MCE was performed before and after dipyridamole infusion in 11 patients with a proximal, significant left anterior descending (LAD) coronary artery stenosis. The relation between contrast-derived parameters and the degree of coronary narrowing and the occurrence of transient regional wall motion abnormalities was also investigated. In the territory supplied by left circumflex coronary artery, mean peak contrast intensity increased after dipyridamole from 50 ± 18 to 76 ± 27 IU (p < 0.001). In contrast, a significant reduction in mean peak intensity was observed after dipyridamole in the LAD territory (from 41 ± 27 to 13 ± 13 IU, p < 0.01). Similar results were obtained with the use of the area under the time-intensity curve. An increase in peak intensity ≥10 IU after dipyridamole administration separated normal regions from those supplied by a significant coronary artery lesion with a sensitivity of 91% and a specificity of 91%. Perfusion abnormalities were always detected by contrast echocardiography when septal motion abnormalities developed and, in five patients they were detected in the absence of clinical, electrocardiographic, and echocardiographic signs of ischemia. A weak correlation was found between both peak intensity and area under the curve and percent coronary diameter stenosis and cross-sectional area. In conclusion, dipyridamole MCE can be used during routine coronary angiography to assess myocardial blood flow distribution in patients with coronary artery disease. The intracoronary injection of contrast agents during dipyridamolestress echocardiography, may provide additional information on the functional significance of coronary lesions, thus helping in prognostic stratification and therapeutic decision making.

Objectives . This study was conducted to assess the efficacy of sulodexide, a glycosaminoglycan compound with antithrombotic properties, in preventing death and thromboembotic events after acute myocardial infarction. Background . Antithrombotic therapy has been found to play an important role in the prevention of cardiovascular events and death after acute myocardial infarction. Glycosaminoglycan-containing compounds, including sulodexide, show profibrinolytic and antithrombotic properties that render them suitable for use in patients after infarction. Methods . A total of 3,986 patients who had recovered from acute myocardial infarction were randomized to receive either the standard therapy routinely administered at each study center, excluding antiplatelet and anticoagulant drugs (control group, 1,970 patients), or the standard therapy plus sulodexide (treated group, 2,016 patients). Between 7 and 10 days after the episode of acute myocardial infarction, sulodexide was administered as a single daily 600-lipoprotein-lipase-releasing unit (LRU) intramuscular injection for the 1st month, followed by oral capsules of 500 LRU twice daily. Patients were evaluated for ≥12 months. Results . At the end of the study, 140 (7.1%) were recorded in the control group and 97 (4.8%) in the sulodexide group (32% risk reduction, p = 0.0022, chi-square test). A total of 90 patients (4.6%) in the control group had a further infarction, compared with 66 (33%) in the sulodexide group (28% risk reduction, p = 0.035). Furthermore, a reduction in left ventricular thrombus formation (evaluated by echocardiography) was observed in the sulodeside group (n = 12; 0.6%), compared with values in the control group (n = 25; 1.3%) (53% risk reduction, p = 0.027). Sulodexide was well tolerated and devoid of significant adverse events. All significant results were confirmed by “actual treatment” analyses. Conclusions . The study provides evidence that long-term therapy with sulodexide started early after an episode of acute myocardial infarction is associated with reductions in total mortality, rate of reinfarction and mural thrombus formation.

Patients with non-Q-wave myocardial infarction (MI) are a heterogeneous population with a wide range of coronary disease severity and extent of myocardial necrosis, showing, therefore, different electrocardiographic findings and different outcomes. To evaluate the role of echocardiography in the management of non-Q-wave MI patients, 192 consecutive patients without previous MI were studied (78 with ST segment elevation, 56 with ST depression and 58 without ST modifications). All patients underwent 2-dimensional echocardiography (16-segment model) within 24 hours of admission to the coronary care unit. Wall-motion abnormalities, wall-motion score index, ejection fraction, and end-diastolic and end-systolic volumes were evaluated. In 35 patients, death, reinfarction, recurrent angina, or severe heart failure occurred during the in-hospital phase, whereas the remaining 157 patients had a good outcome. Patients with a poor prognosis were older (68 +/- 6 vs 59 +/- 5 years, p0.01), had a worse left-ventricular function (wall-motion score index 1.4 +/- 0.4 vs 1.25 +/- 0.3, p0.05; end-systolic volume 54 +/- 25 vs 38 +/- 12 mL/m2, p0.01; ejection fraction 50 +/- 10 vs 58 +/- 8%, p0.01), and presented more frequently with ST segment depression (49 vs 25%, p0.01). The positive and negative predictive values for early clinical events were, respectively: ST segment depression 0.30 and 0.87; wall-motion abnormalities in3 segments 0.28 and 0.86; wall-motion score index1.33 = 0.28 and 0.87; end-diastolic volume46 mL/m2 = 0.49 and 0.91; ST segment depression and wall-motion abnormalities in3 segments 0.60 and 0.88. These results underline the usefulness of echocardiography in the early risk stratification of non-Q-wave MI patients, together with electrocardiographic data. Patients with ST segment depression and more extensive wall-motion abnormalities are at higher risk and their management needs a more aggressive approach.

To investigate whether mitral annular velocity, measured by tissue Doppler imaging (TDI), is able to get a feasible quantitative evaluation of global and regional left-ventricular function during exercise test, 29 patients with previous uncomplicated myocardial infarction were studied by exercise echocardiography. All patients underwent coronary arteriography within 10 days of stress echocardiography. All of them were in sinus rhythm and had no right or left bundle branch block or significant mitral regurgitation as observed by left ventriculography. A total of 12 patients had anteroseptal and/or posteroseptal wall asynergies and left anterior descending involvement; 9 patients had lateral and/or posteroinferior asynergies and left circumflex coronary artery involvement; 8 patients had inferior and posteroseptal wall asynergies and right coronary artery involvement. Twelve subjects of same age and sex with normal cardiovascular findings were selected as a control group. TDI sample volumes were set on the mitral annuli corresponding to anteroseptal, posterior, posteroseptal, lateral, anterior, and inferior wall in 4-chamber, 2-chamber, and long-axis views. There was a significant correlation between the left-ventricular ejection fraction (0.41 +/- 0.8) and the means of the systolic (S) values (6.1 +/- 0.9 cm/sec, r = 0.83, p0.01). The mean S at the sites corresponding to the infarct regions (5.5 +/- 0.4 cm/sec) was significantly lower than the control group (11 +/- 0.8 cm/sec, p0.001). After stress, in patients with multivessel disease, S values corresponding to remote regions were significantly lower (p0.01) compared with control subjects. Thus, the parameters obtained from mitral annular velocities with pulsed TDI in patients with previous myocardial infarction reflect left ventricular asynergy corresponding to the infarct regions and reversible regional dysfunction after exercise.

Experimental evidences underline that hemorheological alterations observed in acute myocardial infarction (AMI) are strictly involved in the decreased perfusion of the damaged area and in the extension of the necrotic regions. We have analyzed whole blood filterability as an index of erythrocyte deformability in 60 AMI patients compared with 30 patients with non-acute coronary artery disease and 52 healthy subjects. Nucleopore polycarbonate membranes with a pore diameter of 5 microm and a filtering pressure of -20 cm H2O were used. The results are expressed as the volume of whole blood filtered in 1 minute (index of filterability, IF). In normal subjects IF was 1.16 +/- 0.24. Among AMI patients IF was 0.70 +/- 0.30 at admission, 0.68 +/- 017 at day 10 and 0.78 +/- 0.14 at day 20. These values were significantly lower than those obtained in normal subjects and in patients with non-acute coronary artery disease. In addition, AMI patients treated with thrombolytic therapy showed, at admission, a significantly higher IF value than that obtained in patients who did not receive thrombolytic treatment (0.85 +/- 0.34 vs 0.60 +/- 0.22; p0.01). These results demonstrate an evident reduction of whole blood filterability in AMI patients that may be considered as an index of erythrocyte deformability. Thrombolytic therapy seems to have a positive effect on blood filterability and may produce beneficial effects through its therapeutical action other than the lysis of the coronary thrombus.

BACKGROUND Inferential evidence suggests that silent ischemia might be related to sympathetic activity. Study of [3H]norepinephrine kinetics is a suitable tool to assess the regional sympathetic activity. This method was applied to investigate whether silent myocardial ischemia in unstable angina is related to and depends on cardiac sympathetic overactivity. METHODS AND RESULTS Patients with active unstable angina were compared with patients with inactive unstable angina, stable effort angina, and controls. Silent myocardial ischemia was evaluated by three 24-hour Holter monitoring periods on alternate days, and [3H]norepinephrine kinetics was assessed under rest conditions and following the cold pressor test. Simultaneously, catecholamine concentrations were measured in the aortic, coronary sinus, and peripheral venous blood. Different than the other groups (p = 0.0013), in patients with active unstable angina, the majority of silent ischemic episodes occurred without increase in heart rate. These patients had a positive coronary sinus-aorta norepinephrine gradient, both at rest and following the cold pressor test. [3H]Norepinephrine kinetics demonstrated an increased selective cardiac spillover, both at rest and, even more, after the cold pressor test. Reduced cardiac [3H]norepinephrine extraction also was found. A significant relation was found between the number of ischemic episodes or the overall duration of silent ischemia and norepinephrine spillover, both at rest and following cold application. CONCLUSIONS During the acute phase of unstable angina (but not in the quiescent phase or in stable effort angina), a disorder in cardiac norepinephrine handling occurs. This results in a reflex cardiac sympathetic overactivity that plays a major role in the occurrence of silent myocardial ischemia.

The value of transthoracic dipyridamole echocardiography has been extensively documented. However, in some patients, because of a poor acoustic window, the rest transthoracic examination is not always feasible and the transesophageal approach is more convenient. Therefore, transesophageal echocardiography with high dose dipyridamole (up to 0.84 mg/kg body weight over 10 min) was performed in 32 patients in whom the transthoracic dipyridamole test either was not feasible (n = 29) or yielded ambiguous results (n = 3). The transesophageal echocardiographic test results were considered abnormal when new dipyridamole-induced regional wall motion abnormalities were observed. All 32 patients underwent coronary angiography; significant coronary artery disease was defined as ≥70% lumen diameter narrowing in at least one major vessel. All patients also performed a bicycle exercise test 1 day before transesophageal dipyridamole echocardiography. Transesophageal stress studies were completed in all patients, with a maximal imaging time (in tests with a negative result) of 20 min. No side effects or intolerance to drug or transducer was observed. The left ventricle was always visualized in the four-chamber and transgastric short-axis views. High quality two-dimensional echocardiographic images were obtained in all patients both at rest and at peak dipyridamole infusion and were digitally analyzed in a quad-screen format. Coronary angiography showed coronary artery obstruction in 24 patients: 6 had single-, 9 double- and 9 triple-vessel disease. The transesophageal dipyridamole test showed a specificity of 100% and an overall sensitivity of 92%. The sensitivity of this test for single-, double- and triple-vessel disease was 67%, 100% and 100%, respectively. It is concluded that transesophageal dipyridamole echocardiographic testing is a useful detector of myocardial ischemia in patients with coronary artery disease, particularly in those in whom a transthoracic study either is not feasible or yields ambiguous results.

The aim of this study was to assess the presence of Chlamydia pneumoniae antibodies in patients with angiographically verified atherosclerotic coronary artery disease. A total of 114 consecutive patients were investigated between April 1995 and June 1996. Patients were divided into two groups: 72 patients with acute myocardial infarction (AMI; 53 men, 19 women, mean age 62.27 +/- 10.1 years), and 42 patients with chronic ischemic heart disease (CAD; 37 men, 5 women, mean age 62.75 +/- 9.2 years). A control group of 50 normal subjects matched for age (mean 62 +/- 9 years), sex, social status and geographical area was used. Identification of Chlamydia pneumoniae was carried out with the microimmunofluorescence method, on two serum samples taken from patients on admission and after 15 days. The IgM, IgG and IgA anti-Chlamydia pneumoniae titers were assessed, valuesor = 1:16,or = 1:32 andor = 1:8 being respectively considered positive. Acute (IgMor = 16 or four fold rise of IgG titer) and chronic (IgGor = 128 e IgAor = 32 or only elevated IgA titer) infections were analyzed. IgM antibodies were not found in AMI, CAD and control groups. IgG positivity (IgGor = 32) was found in 38% of the control group, in 58.3% of the AMI group (p0.05) and 42.8% of the CAD group (p0.01). IgA positivityor = 8) was found in 22% of the control group, in 31.9% of the AMI group (NS) and in 33.3% of the CAD group (por = 0.05). Acute infection was observed in 5.5% of AMI patients and in 12% of CAD patients (NS), whereas no subject of the control group showed these values. Chronic infection was observed in 9.7% of AMI patients and in 16.6% of CAD patients (NS) whereas nobody of the control group showed these values. In conclusion, our results suggest that Chlamydia pneumoniae infection is present only in the AMI and CAD groups. It is possible to suppose that this infection may be linked to atherosclerosis through an endothelial damage or a systemic endogenous procoagulant and inflammatory activity.

The clinical arena in which we must consider the role of echocardiography is characterized by 2 fundamental findings: (1) most patients with chest pain and suspected acute myocardial infarction (MI) do not present diagnostic electrocardiograms; and (2) an early and correct diagnosis is necessary to match the patient with the most adequate treatment. Echocardiography may be very useful in the coronary care unit, allowing a correct diagnosis of ischemic heart disease when electrocardiography is unclear, even before the rise of cardiac enzymes is detected. It may also play a role in decision-making for thrombolytic therapy. In addition, echocardiography provides useful information for early risk stratification. In fact, although high-risk patients are well identified by simple clinical or instrumental variables (i.e., Killip classification, enzymatic data, blood-gas analysis, electrocardiogram, etc.), most patients (>60%) are identified as low risk, and several subjects classified into the low-risk groups have a poor prognosis and are not detected using a single variable. In our experience, 2-dimensional echocardiography was able to further stratify between patients of low-risk classes. Therefore, echocardiography plays an important role in the early stratification of acute MI patients, especially in those without signs or symptoms of heart failure.

Background Supine bicycle exercise echocardiography (SBEE) has never been used before and early after percutaneous transluminal coronary angioplasty (PTCA) for assessing the functional outcome of the procedure and predicting late restenosis. Methods and Results We selected 76 subjects with stable angina, normal wall motion at rest, and exercise-induced wall-motion abnormalities before PTCA. SBEE with peak exercise imaging and the use of a 16-segment, four-grade score model was performed 54±15 hours after PTCA. No exercise-related adverse events occurred. Patients were grouped according to SBEE results: group 1 (n=35, 46%) with negative exercise ECG and echo; group 2 (n=19, 25%) with a positive exercise ECG but normal echo; and group 3 (n=22, 29%) with a positive exercise echo with either a positive (n=7, 32%) or negative (n=15, 68%) ECG. Exercise performance significantly improved in all groups. In group 3, peak wall-motion score index decreased from 1.27±0.11 before to 1.15±0.06 after PTCA ( P P 50%) was 37%. By multiple logistic regression analysis, clinical restenosis was associated with a positive post-PTCA exercise echo (odds ratio [OR] 3.08, 95% confidence interval [CI] 1.66 to 5.72; P =.0004) and with increasing values of pre-PTCA wall-motion score index (OR 2.86, 95% CI 1.92 to 4.27; P =.005) and duration of wall-motion abnormalities (OR 2.12, 95% CI 1.07 to 4.20; P =.04). Conclusions SBEE is a safe and reliable tool to demonstrate changes in exercise-induced wall-motion abnormalities after PTCA and provides prognostic information in the risk assessment of clinical restenosis.

Although several studies have investigated left ventricular (LV) function after reperfusion inter ventions, it is still unclear whether benefits result from successful therapy or whether such benefits only reflect the natural history of a subgroup of patients with acute myocardial infarction (AMI). This study evaluates the unique effect of thrombolytic therapy on the natural history of regional LV wall motion dysfunction. One hundred seventy-six patients with AMI were studied: 82 patients (group A) underwent conventional treatment and 94 (group B) thrombolytic therapy. LV regional improvement, evaluated by changes in echo score between admission and predischarge examination, was present more frequently in group B (28%) than in group A (17%). Furthermore, improved patients in group B had higher admission echo scores (7.5 ± 3.5 vs 6.3 ± 3.1), a prevalence of anterior AMI (68 vs 30.1%) and a higher rate of coronary patency (92 vs 58% in patients who had no improvement). In group A patients the rate of coronary patency was similar in those who did (46.1%) and did not have (36.1%) improvement. Observations at 12 to 18 months showed similar data in group A patients and in group B patients without improvement, whereas a marginal additional improvement was observed in group B patients who had in-hospital improvement. These observations demonstrate that LV function recovery is more frequent and marked in treated than in untreated patients. Follow-up results suggest a prolonged beneficial effect of thrombolytic treatment on LV function. The highest rate of coronary patency in improved group B patients underline the role of reperfusion on natural history of LV dysfunction after AMI.

Plasma β-endorphin levels provide controversial results on the role of endogenous opioid system in modulation of anginal pain. As an alternative, the action of plasmatic luteinizing hormone after administration of naloxone was investigated: naloxone blocks the tonic endogenous opioid system inhibition of gonadotropin release; thus, the level of luteinizing hormone after naloxone administration is an index of central endogenous opioid system activity. Twenty patients with coronary artery disease and positive results of stress tests were selected: 10 had angina (group I) and 10 did not (group II). Ten healthy subjects were also studied as a control group (group III). In all patients basal plasma β-endorphin levels, basal luteinizing hormone plasma levels (every 15 minutes for 1 hour) and luteinizing hormone plasma levels after administration of 0.1 mg/kg naloxone over 4 minutes (every 15 minutes for 2 hours) were determined. In 15 patients the test was performed after luteinizing hormone releasing hormone was given. The integral concentration time of luteinizing hormone plasma level during baseline (LHiB) and after administration of naloxone (LHiN) or luteinizing hormone releasing hormone (LHiRH), the ratio (LHiN:LHiB and LHiRH:LHiB) and the differences (LHiN-LHiB and LHiRH − LHiB) between the postinfusion period and baseline were calculated. No difference was found in β-endorphin plasma levels and luteinizing hormone response after luteinizing hormone releasing hormone infusion. On the contrary, after naloxone administration, group II showed significantly higher responses (LHiN − LHiB, 2413 ± 380 mlU/ml; LHiN:LHiB, 5 ± 0.4) with respect to group I (LHiN − LHiB, 1150 ± 304 mlU/ml; p p p p

Many authors have shown an association between Chlamydia pneumoniae (C. pneumoniae) infection and coronary artery disease. However, whether C. pneumoniae infection plays an important role in triggering an acute coronary event remains to be elucidated.Sixty-four consecutive patients with unstable angina (group A), 56 consecutive patients with stable exertional angina (group B) and 74 control subjects (group C) were studied. The IgM, IgG and IgA anti-C. pneumoniae titers were assessed (microimmunofluorescence test Labsystem), valuesor =1:16,or =1:32 andor =1:16 being respectively considered positive.IgM antibodies were found in 10.9% of group A and 12.5% of group B patients, whereas no subject of group C showed IgM titers (A vs. B, p=ns; C vs. A and B, p0.05). Positive IgG titers were found in 76.6%, 82% and 44.6% in groups A, B and C, respectively (A vs. B, p=ns; C vs. A and B, p0.05). Positive IgA titers were found in 62.5%, 61% and 31.1% in groups A, B and C, respectively (A vs. B, p=ns; C vs. A and B, p0.05). Acute infection was observed in 10.9% and 12.5% of patients in groups A and B, respectively (p=ns); reinfection in 17% and 11%; no patient of the control group had signs of acute infection or reinfection. Chronic infection was observed in 34.4% and 37.5% in group A and B, respectively (p=ns).C. pneumoniae infection is associated with coronary artery disease, but no difference in serology is present between unstable and stable angina. Therefore, it does not seem implicated in triggering an acute coronary event.

AIMS The aim of this study was to analyse the relationship between infarct-related artery residual stenosis, assessed by quantitative coronary angiography, and left ventricular function changes during the in-hospital period in patients with acute myocardial infarction undergoing thrombolytic treatment. METHODS AND RESULTS The study population consisted of 90 patients with acute myocardial infarction treated with thrombolysis within 6 h of the onset of symptoms. Left ventricular function was serially assessed by an echocardiographic asynergy score (before thrombolysis and pre-discharge). Left ventricular end-diastolic and end-systolic volumes were also calculated. Coronary stenosis was evaluated by computer-assisted videodensitometric analysis at pre-discharge coronary angiography. Three subgroups were identified on the basis of left ventricular function changes: 25 patients (Group A) with regional myocardial improvement (echo score from 7.5 +/- 3.5 to 4.3 +/- 3.2), 51 (Group B) with no variation in echo score (4.8 +/- 2.7) and 14 (Group C) with myocardial regional worsening (echo score from 4.4 +/- 2.1 to 8.8 +/- 2.4). Group A patients exhibited a very high incidence of infarct-related artery patency (23/25 patients, 92%) vs 71% with unchanged (Group B) and 14% (Group C) with worsening regional left ventricular function (P < 0.001). Subdivision of the study population on the basis of residual stenosis severity showed that a significant improvement in left ventricular function was present only in the subgroup with residual stenosis < 75% (echo score from 5.2 +/- 3.4 to 3.6 +/- 2.9, P < 0.001). CONCLUSION These results support the important role exerted by complete coronary patency after thrombolysis in inducing left ventricular function recovery, and the poor functional improvement in patients with incomplete coronary patency.

In order to assess the role of the pulmonary venous flow (PVF) velocity pattern in the evaluation of patients with congestive heart failure (CHF), we studied 41 CHF patients by means of transthoracic echocardiography (TTE) and multiplane transesophageal echocardiography (TEE). The etiology of CHF was idiopathic or ischemic dilated cardiomyopathy in 19 patients and hypertensive heart disease in 22. Sixteen subjects without cardiovascular disease were selected as normal controls. PVF peak systolic and peak early diastolic (D) velocities were recorded by TEE and TTE and the systolic fraction (SF) was measured (i.e., the systolic velocity-time integral-VTI-expressed as a fraction of the sum of systolic and early diastolic (VTI). TEE tracings were obtained in all patients and had more laminar-appearing spectral signals, thus were used for analysis. By TEE the mitral flow velocity patterns were also evaluated: peak early diastolic velocity (E), peak velocity at atrial contraction, E velocity normalized for VTI (E/VTI), deceleration time (DT), and left ventricular isovolumic relaxation time (LVIRT). The left ventricular ejection fraction (LVEF) was calculated by two-dimensional echocardiographic images using the modified Simpson method. The SF was lower in CHF patients as compared with normal controls (p0.0001). The E/VTI ratio was higher, and DT and LVIRT were shorter (p0.0001) in CHF patients. A significant correlation was observed between SF and LVEF in CHF patients (r = 0.76, p0.001). Two different PVF velocity patterns (type A:SF50%, D50 cm/s; type B:SF approximately 50%, D50 cm/s) were recognized in patients with a low LVEF (type A) and a nearly normal or normal LVEF (type B). Patients with LVEF40% showed mean SF values significantly lower than patients with LVEF40% (33.26 +/- 10.84 vs. 51.00 +/- 4.00%, p0.0001). Mean DT and LVIRT values were not significantly different in patients with LVEF40% and40%. Thus in CHF patients TEE PVF velocity patterns help in distinguishing patients with systolic dysfunction (low LVEF and SF) from patients with predominant diastolic impairment (normal or nearly normal LVEF, high D velocities).

The aim of this study was to evaluate, in a large series of patients (420 males, 104 females, mean age 59 +/- 9.4 years) with acute myocardial infarction (AMI), the role of electrocardiography and two-dimensional echocardiography in identifying the site and the extension of the necrotic area, with regard to the treatment (thrombolysis or not) and the extent of coronary artery disease. Our results have shown a good correlation between ECG and echo in evaluating the infarct size, with a larger extension in echo examinations. Regarding the infarct site, a good correlation was found in anterior AMI, but not in inferior AMI. Thrombolytic therapy does not seem to introduce significant variations in this regard. Furthermore, the results of coronary angiography have shown that two-dimensional echocardiography allows us to identify the infarct-related coronary artery in a larger number of patients (90%) compared to ECG (80%). On the contrary, the two methods are similar in evaluating the extent of coronary artery disease, with correct identification of only one third of patients, the majority of them with single-vessel disease. Finally, we observed that the presence of abnormal apical wall motion is frequent (47%), in the majority of cases associated with anterior wall motion abnormalities, while in 5% of the cases the apex alone is involved. This finding suggests an analogy between these "apex infarctions" and the non Q wave infarctions, in which necrosis is present only in a little zone of a larger area at risk.

Aim of this study was to assess the behaviour of left ventricular volumes during dobutamine echocardiography in patients with coronary artery disease (CAD) compared to subjects with normal coronary angiograms. We have measured the end-diastolic and end-systolic volumes and a non invasive index of myocardial contractility (the ratio between systolic blood pressure and end-systolic volume index, SBP/ESVI) in 67 patients undergoing dobutamine echocardiography and quantitative coronary angiography. Patients were divided into 3 groups: Control group (n = 10) without CAD; Group I (n = 30) with CAD but normal resting wall motion; Group II (n = 27) with CAD and resting wall motion abnormalities. Volumetric response to dobutamine was deemed abnormal when percent changes of left ventricular volumes from baseline to peak infusion were below 2 standard deviations of the mean values obtained in the control group. The normal or pathological volumetric response was compared with the extent of significant (70% lumen stenosis) coronary artery disease. In the control group, dobutamine produced a significant decrease in both end-diastolic and end-systolic volumes, with percent changes from rest to peak of 24 +/- 5% and 29 +/- 5% respectively, and an average increase of 70 +/- 20% in the SBP/ESVI ratio. Among the 22 Group I patients who showed dobutamine-induced asynergies, volumetric response in those with multivessel disease was normal in 5/14 (36%) and abnormal in 7/8 (87%, p0.05), whereas among the remaining 8 patients who had no dobutamine-induced asynergies, an abnormal volumetric response was always associated with multivessel disease (n = 3/3, 100%). In Group II, the prevalence of abnormal volumetric responses in the presence (n = 15) or absence (n = 12) of dobutamine-induced new or worsening asynergies was respectively 92% and 87% in patients with multivessel disease, whereas in those with single vessel disease the prevalence was lower, although not significantly (8 and 13%, p = 0.08 vs multivessel CAD). Predictive accuracy of an abnormal volumetric response for identifying multi-vessel coronary artery disease in Groups I and II was not significantly different (77 and 85%, respectively, NS). Our preliminary data indicate that the evaluation of left ventricular volumes during dobutamine echocardiography yields additional information on myocardial intropic reserve, useful for diagnostic and functional assessment of patients with coronary artery disease. Moreover, this study emphasizes the importance of defining the "normal" left ventricular performance during DE to be able to regard an abnormal volumetric behaviour as a reliable marker of impaired inotropic reserve.

We have studied 455 consecutive patients with acute myocardial infarction to assess the early and mid-term prognostic value of clinical and laboratory findings in the acute (i.e. Killip classification, arterial PO2, echocardiographic extent of necrotic area) and subacute phase (exercise test, ambulatory ECG). Results showed that clinical examination, blood gas analysis and two-dimensional echocardiography have a high predictivity for in-hospital risk stratification. In particular, two-dimensional echocardiography showed that patients with diffuse wall motion abnormalities had a worse prognosis during the follow-up. Exercise test and, to a lesser extent, ambulatory ECG have well identified patients at risk for new coronary events.

The present study, selecting 39 patients undergoing elective coronary angioplasty (PTCA) with signs of myocardial ischemia during supine bicycle exercise stress test (EST) before PTCA and on medical therapy, was designed: to evaluate the efficacy of angiographically successful PTCA on functional capacity, in terms of work load, time of exercise and rate-pressure product (RPP), by comparing pre- and post-PTCA-EST performed in patients with post-PTCA disappearance (Group I, 44%) or persistence (Group II, 56%) of myocardial ischemia, and in the latter, to evaluate the effects of medical therapy, by repeating EST after its addition; to investigate the influence of PTCA on regional function, assessed by a 11 segment model and graded as usual, in the 25 patients group with pre-PTCA exercise-induced wall motion abnormalities, disappearing (Group A, 64%) or persisting (Group B, 36%) after the interventional procedure; to examine by a 12-month follow-up the eventuality of recurrent anginal symptoms, in the presence of myocardial ischemic signs in the territory supplied by the dilated vessel and/or of angiographic restenosis, in relation to the result of post-PTCA-EST. The results of our study showed a significant improvement in functional capacity after PTCA only in Group I patients, whereas in Group II patients effort tolerance significantly increased only after medical therapy, which was associated with the disappearance of myocardial ischemia. With regard to follow-up, exercise echocardiography showed a positive and negative predictive value for angina recurrence with angiographic restenosis of 78 and 92%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Objectives. This study used myocardial contrast echocardiography to investigate the extent of residual perfusion within the infarct zone in a select group of patients with recently reperfused myocardial infarction and evaluated its influence on the ultimate infarct size. Background. Limited information is available on the status of myocardial perfusion within postischemic dysfunctional segments at predischarge and on its influence on late regional and global functional recovery. Methods. Twenty patients with acute myocardial infarction were selected for the study. Patients met the following inclusion criteria: 1) single-vessel coronary artery disease; 2) patency of infarct-related artery with persistent postischemic dysfunctional segments at predischarge; 3) stable clinical condition up to 6 months after hospital discharge. All selected patients underwent coronary angiography and myocardial contrast echocardiography before hospital discharge and repeated the echocardiographic examination 6 months later. Patients were grouped according to the pattern of contrast enhancement in predischarge dysfunctional segments. Results. In nine patients (group I), the length of segments showing abnormal contraction coincided with that of the contrast defect segments. In the remaining 11 patients (group II), postischemic dysfunctional segments were partly or completely reperfused. There was no difference between the two groups in asynergic segment length at predischarge (7.3 ± 2.5 vs. 7.2 ± 4.3 cm, p = NS). At follow-up study, asynergic segment length was significantly reduced in group II patients, whereas no changes were observed in group I patients (from 7.2 ± 4.3 to 4.7 ± 3.7 cm, p < 0.005; and from 7.3 ± 2.5 to 7.5 ± 2.9 cm, p = NS, respectively). Conclusions. Among patients with a predischarge patent infarct-related artery, further improvement in regional and global function may be expected during follow-up when residual perfusion in the infarct zone is present.

To assess the prognostic significance of supraventricular tachyarrhythmias (SVTA) during acute myocardial infarction (AMI), we studied 388 patients with first AMI, without ventricular preexcitation or chronic atrial fibrillation. The prevalence of SVTA was 14% (56/388), including atrial fibrillation (57%), atrial flutter (22%), polyfocal atrial tachycardia (14%), monofocal atrial tachycardia (7%). The arrhythmia appeared within 72 hours from the onset of chest pain in 61% of patients (early SVTA72 hours), while in 39% appeared later (late SVTA72 hours). Patients with SVTA (Group I n = 56) and without SVTA (Group II n = 232) were similar regarding prevalence of hypertension, dyslipidemia, diabetes, site of infarction and fibrinolysis, but SVTA was associated with a significant increase in death (Group I 18% versus Group II 9%; p0.05) and complications as pulmonary oedema and cardiogenic shock (Group I 25% versus Group II 14%; p0.05). Left atrial dimensions (LAD), end-diastolic left ventricular volume (EDLVV), end-systolic left ventricular volume (ESLVV) and echo-score, evaluated at admission, were not different between Group I and II (LAD 41.3 +/- 6 mm versus 40.1 +/- 5 mm, NS; EDLVV 181 +/- 34 ml versus 173 +/- 30 ml, NS; ESLVV 80 +/- 21 ml versus 75 +/- 18 ml, NS; echo-score 6.7 +/- 3.1 versus 6 +/- 2.7, NS) while pre-discharge echo-grams in Group I showed a trend towards the increase in volumes and echo-score (EDLVV from 181 +/- 34 ml to 194 +/- 36 ml, p = 0.052; ESLVV from 80 +/- 23 ml to 88 +/- 23 ml, p = 0.051; echo-score from 6.7 +/- 3.1 to 7.8 +/- 3.3, p = 0.070).(ABSTRACT TRUNCATED AT 250 WORDS)

Although heart rate variability is a very important prognostic factor in patients with myocardial infarction, the mechanism for the reduction in the vagal cardiac activity is unknown: myocardial infarction can cause local areas of sympathetic or parasympathetic denervation that leads to catecholamine hypersensitivity; the destruction of local ventricular receptors of the autonomic system may alter feedback to the higher centres, impairing autonomic regulation; the mechanical distortion consequent to the infarction can give rise to sympathetic overactivity. Effective thrombolysis in myocardial infarction could reduce myocardial necrosis and, therefore, cause less reduction of vagal activity and/or less sympathetic stimulation. To determine whether systemic thrombolysis has some effect on heart rate variability we studied 40 patients with a first transmural myocardial infarction. Enrollment criteria were very strict: all the patients with conditions potentially influencing heart rate variability were excluded from this study. Between day 15 and day 25 from the infarction patients had an Holter monitoring. A program we developed provided for the automatic identification of R wave, for the calculation of RR interval, and for the recognition of pause, extrasystolic and post-extrasystolic beats, that could be thus excluded from the analysis. Patients were divided in 2 groups: 17 patients treated with thrombolysis and 23 subjects treated traditionally. There were no difference between the 2 groups with regard to the age and cardiac function, except for the less echo score in the fibrinolytic treated group.(ABSTRACT TRUNCATED AT 250 WORDS)

By using a highly sensitive, high-performance liquid Chromatographic technique, plasma values of malondialdehyde (MDA), adenosine and oxypurines were determined in 10 healthy subjects, 10 patients with noncardiac illness, and 20 patients with acute myocardial infarction (AMI) observed within 6 hours from the onset of symptoms. Patients with AMI received fibrinolytic treatment. Peripheral blood was obtained before and serially after thrombolysis (1, 2, 3, 6 and 24 hours). Coronary patency was assessed by timing of peak creatine phosphate kinase and by predischarge angiography. MDA (mean ± SD) in healthy subjects, noncardiac patients, and immediately before thrombolytic treatment in patients with AMI was 0.051 ± 0.013, 0.066 ± 0.020 and 0.397 ± 0.326 μmol/liter of plasma, respectively. A progressive increase in plasma MDA after thrombolysis was observed only in reperfused patients, whose values at the third, sixth and 24th hours were also significantly greater than those of nonreperfused patients. Time-dependent variations of xanthine and adenosine were also observed in the same group after thrombolysis. The data appear to indicate that a relevant increase in plasma MDA, mostly originating due to phospholipid derangement of postischemic myocytes, occurs only in patients with successful thrombolysis, thus suggesting that if properly assayed, it may represent reliable biochemical evidence of tissue injuries after myocardial reperfusion in humans.

Five hundred twenty-nine patients with acute myocardial infarction (AMI) underwent clinical, enzymatic and echocardiographic evaluation. Two-dimensional echocardiography identified 71 patients with left ventricular thrombus (LVT): 63 males and 8 females; mean age 54 +/- 12 years; 70 with anterior AMI and 1 with inferior AMI. The incidence of LVT was 13.8% and 27.7% among anterior AMI. At admission to Coronary Care Unit the patients with LVT showed more extensive left ventricular dysfunction than patients without LVT: Killip classificationor = 2 was 54.5% versus 41.4%, p0.05; peak of creatinphosphokinase was 1337 UI/L versus 951 UI/L, p0.05; echo-score was 7.2 +/- 2.8 versus 4.7 +/- 3.5, p0.01. Serial echocardiograms showed disappearance of LVT in 24 patients. Regarding regional wall motion abnormalities, patients with LVT disappearance showed lower pre-discharge echo-scores than patients with LVT persistence (6.7 +/- 2.2 versus 8.4 +/- 2.9; p0.01) although echo-scores at admission were similar in the 2 groups (7.1 +/- 1.1 versus 7.3 +/- 3.4, NS). These results suggest: the importance of extension of myocardial infarction and left ventricular dysfunction in LVT evolution; the importance of treatment limiting infarct size and improving left ventricular function, such as thrombolytic therapy. Anticoagulant therapy could be limited to patients with higher risk of embolization (as the protruding shape of LVT).

In order to test MRI ability to detect the number and the sites of coronary artery by-pass grafts (CABGs), 22 patients with CABGs were studied. The detection of a neo-vessel in even one of the examination slices was considered as positive for the study, disregarding the difference between its origin and course. With such a criterion, MRI total percentage of vascular bridges identification resulted in 76.1% (51/67) with very low values for CABGs implanted on diagonal, obtuse marginal and posterior descending vessels (11/24 = 45.8%). These results lead to the conclusion that, although MRI has some advantages in the identification of CABGs implanted on the main coronary vessels in the early post-operative period, its extensive use cannot be proposed at the present state of the art.

Early relaxation is characterized by a segmental outward wall movement during isovolumic relaxation. There is still no general agreement as to its significance. Some Authors have considered the phenomenon to be a specific marker of isolated coronary narrowing, others have regarded it as a normal variation of left ventricular relaxation and still others concluded that it is a compensatory phenomenon to local ischemia in another region. We used a method of quantitative assessment of regional left ventricular function and a videodensitometric analysis of coronary stenosis. In our study we didn't observe an improved systolic function of the regions that presented early relaxation, but a slight non significant reduction. We did neither observe any correlation between early relaxation and ischemia provoked by stress test nor between early relaxation and coronary artery disease. The amplitude of early relaxation was not statistically different between patients with and without stenosis of left anterior descending artery. We conclude that early relaxation is a normal variation of left ventricular relaxation.

In order to understand the effect of LVEDP changes caused by contrast injection during angiography on coronary hemodynamics we studied 15 patients (5 congestive CMP, 5 mixed angina and 5 controls). Our results do not cope with an important negative role played from LVEDP changes on coronary hemodynamics and cardiac metabolism. Actually LVEDP increase after ventriculography was balanced by coronary flow increase and impedance reduction even when the latter has been matched with LVEDP. We also observed lactate metabolism changes which are not likely to be provoked by myocardial ischemia, since there was not a definite negativization of % lactate extraction and delta A-VO2 always turned to reduction; this is apparently not in agreement with other Authors who had reported metabolic alterations suggestive for myocardial ischemia, even if they did not calculate delta A-VO2 and coronary flow. This difference could be related to the different populations studied, specially when considering the different functional meaning of coronary stenoses of the same degree at angiography. Is thus the Authors' thought that, when coronary reserve is still adequate, is it possible not to take into account LVEDP, which becomes important in patients with a more advanced coronary disease as in those cases this extravascular impedance factor to coronary flow could take his own worsening role.

In order to investigate whether coronary vasodilating prostaglandins (PGI2 and PGE2) have a role in the pathophysiology of myocardial ischemia, 26 patients with angina pectoris and 23 control subjects (nonischemic patients) were studied by assessing coronary hemodynamics and prostaglandin formation in relation to sympathetic stimulation. Following a cold pressor test (CPT), coronary prostaglandin output markedly increased (p less than 0.001) and coronary vascular resistance (CVR) decreased (p less than 0.001) in all control subjects. In contrast, in anginal patients prostaglandins in the coronary sinus were undetectable and after CPT prostaglandin output did not increase, whereas CVR paradoxically increased (p less than 0.001). In control subjects the inhibition of coronary prostaglandin formation (by ketoprofen [1 mg/kg intravenously] or by aspirin [15 mg/kg intravenously]) caused a paradoxical increase of CVR following CPT (p less than 0.001). In anginal patients the inhibition of prostaglandins further exaggerated the increase of CVR after CPT (p less than 0.001). These results indicate that coronary vasodilating prostaglandin PGI2 and PGE2 play a role in modulating coronary vascular response to sympathetic stimulation induced by CPT. Their defective production in anginal patients may be responsible for the paradoxical increase in CVR following sympathetic stimulation.

To assess the relation between the extent of myocardial necrosis and the presence of myocardium at risk in myocardial infarction without Q waves (NQMI) we studied by echocardiography the prevalence of jeopardized myocardium in a group of NQMI stratified on the basis of left ventricular wall motion (akinesis, hypokinesis, normal kinesis). We have studied 60 consecutive patients with non-Q myocardial infarction. Patients were examined by 2D echo at rest (V-VI day from the acute episode) and during symptoms limited bicycle ergometric test (ExT) (XX-XXX day). Regional left ventricular wall motion was evaluated as normal or asynergic (severe hypokinetic, akinetic) and the ExT was considered positive in case of new asynergic areas or ECG criteria. 2D echo at rest was technically satisfactory in 56 patients, 19 showed almost an akinetic segment (Aci) 17 had hypokinetic areas (Ipo) and 20 had normal left ventricle kinesis (Norc). Wall motion abnormalities were localized more frequently in the apex and lateral areas. During exercise 2D echo was performed in 46 patients (82%) with 23 positive tests (50%). Stratifying the population on the basis of left ventricle wall motion we observed a major number of positive tests in the group of patients with normal wall motion in comparison with those with asynergic areas at rest (Norc 66.6%, Ipo 35.7%, Aci 42.6% p less than 0.05 Nore vs Ipo and Nore vs Aci) despite the same CAD extension. These data show the heterogeneity of the NQMI that likely includes patients with transmural (asynergy group) and subendocardial MI (normal kinesis group), the latter with a higher degree of myocardium at risk.

To investigate a physiologic role of coronary prostacyclin (PGI2) and prostaglandin E2 (PGE2) 30 patients who were not affected by coronary heart disease were evaluated for coronary hemodynamics and coronary PGI2 and PGE2 production. Inhibition of coronary prostaglandin biosynthesis by ketoprofen (1 mg/kg) or aspirin (15 mg/kg) administered intravenously did not significantly change coronary hemodynamics in resting conditions. In all patients cold pressor tests induced significant increases in coronary blood flow (p less than 0.001) and decreases in coronary vascular resistance (p less than 0.001) without changes in cardiac oxygen extraction and with consequent increases in calculated myocardial oxygen consumption. Simultaneously, a marked increase in coronary PGI2 (as 6-keto-PGF1 alpha) and PGE2 formation was observed (p less than 0.001). Both ketoprofen (1 mg/kg) and aspirin (15 mg/kg) administration completely abolished PGI2 and PGE2 formation that was induced by cold pressor test and caused a paradoxical increase in coronary vascular resistance (ketoprofen: p less than 0.02; aspirin: p less than 0.05). The results of this study support a physiologic role for the coronary prostaglandins in modulating coronary vascular response to sympathetic stimulation in nonischemic patients.

Two-dimensional and Doppler echocardiographic studies and a hemodynamic investigation were performed during dipyridamole testing in 42 subjects (13 control subjects and 29 patients with coronary artery disease [CAD]), to evaluate the ability of dipyridamole Doppler echocardiography in identifying patients with ischemic left ventricular dysfunction. In the control group, after dipyridamole infusion, Doppler-derived parameters increased significantly from baseline (p less than 0.001). In patients with CAD, peak flow velocity, flow velocity integral and stroke volume failed to increase after dipyridamole infusion (0.89 +/- 0.21 to 0.85 +/- 0.18 m/s, difference not significant; 14 +/- 3 to 12 +/- 4 cm, difference not significant, and 56 +/- 13 to 50 +/- 14 ml/beat, p less than 0.05, respectively). Heart rate, rate pressure product, systemic vascular resistance and mean right atrial pressure had similar variations in the 2 groups. Changes in the 3 Doppler-derived parameters are closely related to the variations of peak positive dP/dt, stroke volume (thermodilution) and left ventricular end-diastolic pressure and are closely related to the coronary angiography jeopardy score and to the appearance of wall motion abnormalities. Thus, by combining Doppler and 2-dimensional echocardiography, dipyridamole-induced myocardial ischemia may be detected in a high percentage of CAD patients, providing a sensitive tool for identifying patients with high-risk coronary artery anatomy.

After treatment with alpha-methyldopa a regression of left ventricular hypertrophy, due to hypertension, has been reported in spontaneously hypertensive rats. The reduction of left ventricular mass has been associated with an increase in hydroxyproline concentration, suggesting secondary functional changes. On this basis, 12 patients with essential hypertension and echocardiographic evidence of left ventricular hypertrophy have been studied before and after a 6-month alpha-methyldopa treatment. Ten normal subjects were used as a control group. Curves of changes in left ventricular diameter and velocity curves were obtained by digitation of the M-mode endocardial echoes and the diastolic patterns were studied. Before treatment all patients, as compared to normal subjects, showed: (a) prolongation of the isovolumetric relaxation time index, with increased diameter changes; (b) reduction of diameter changes and peak velocity during the rapid filling; and (c) marked compensatory increase of diameter changes and peak velocity of the filling due to atrial systole. Left ventricular hypertrophy was reduced in 5 patients (first group) after treatment. This group showed: (a) normalization of the isovolumetric relaxation time index; (b) slight increase of diameter changes during rapid filling; (c) increased peak velocity of the rapid filling; and (d) reduction of diameter changes and peak velocity during atrial systole. No changes of functional data were observed in the other 7 patients (second group) in whom left ventricular hypertrophy was unchanged after treatment. It is shown how the reduction of left ventricular hypertrophy, per se, could induce such an improvement of diastolic function, despite the biochemical changes probably caused by administration of alpha-methyldopa.

Objectives. This study sought to compare the impact of primary coronary angioplasty and thrombolytic therapy for acute myocardial infarction (AMI) on 1-month infarct size and microvascular perfusion.Background. The effect of the reperfusion strategies of primary coronary angioplasty and thrombolytic therapy on microvascular integrity still remains to be determined.Methods. Sixty-two consecutive patients with a first AMI, undergoing intravenous tissue-type plasminogen activator (t-PA) therapy (32 patients, Group I) or primary angioplasty (30 patients, Group II), were studied. Only patients with 1-month Thrombolysis in Myocardial Infarction (TIMI) flow grade 2 or 3 were selected for the study. Patients in whom primary angioplasty was unsuccessful or those with clinical evidence of failed reperfusion were excluded. Microvascular perfusion was assessed at 1 month by intracoronary injection of sonicated microbubbles. Contrast score index (CSI) and wall motion score index (WMSI) were derived using qualitative methods.Results. At baseline there were no significant differences between groups for age, risk factors, time to hospital presentation, Killip class on admission, prevalence of multivessel disease or anterior infarct site, infarct area extension before reperfusion, peak creatine kinase levels and postinfarction treatment. Conversely, significant differences between groups were found at follow-up for percent residual infarct related-artery (IRA) stenosis (70 ± 12 vs 36 ± 14 [mean ± SD], p = 0.0001), CSI (1.02 ± 0.4 vs. 1.49 ± 0.5, p = 0.0003) and WMSI (1.67 ± 0.3 vs. 1.45 ± 0.3, p = 0.015). In particular, in the subset of patients with TIMI grade 3 flow, a perfusion defect occurred in one or more segments subtended by the IRA in 72% of Group I versus 31% of Group II patients (p < 0.00001) and in 27% of Group I versus 8% of Group II segments (p < 0.00001).Conclusions. The present study shows, in a highly selected cohort with successful IRA recanalization, that primary angioplasty is more effective than thrombolysis in preserving microvascular flow and preventing extension of myocardial damage at 1-month after AMI.

Risk stratification is mandatory in the management of the postinfarction period. The identification of high-risk patients, on the basis of clinical data (recurrent angina, overt heart failure, etc.), is quite easy, whereas stratification of uncomplicated subjects needs an accurate noninvasive strategy. In the last 20 years, echocardiography has been gaining an increasing role, allowing increasingly precise evaluation of infarct size. This detection of the extent of infarct size has a definite prognostic value. Since 1980, we have observed that a dysfunctioning left ventricular myocardium >40% marked patients with a poor prognosis. These observations are most important in asymptomatic infarct patients, in whom clinical features may not reflect the amount of left ventricular dysfunction. Our recent results on a large series of patients with acute myocardial infarction (MI) without overt heart failure have shown that the extension of wall motion abnormalities at 2-dimensional (2D) echocardiography was highly predictive of cardiac death or new coronary events in a 3-year follow-up (univariate analysis; p

The mechanism responsible for the absence of anginal pain in patients who have episodes of both painless and painful myocardial ischemia, still remains unknown. Does the pain depend on an overstimulation of receptive structures or is this symptom the product of the excitation of a well-defined receptive system? The aim of this work is to test the first hypothesis: whether silent attacks are accompanied by the same degree of mechanical impairment as symptomatic ones. The authors compared the echocardiographic left ventricular functional behavior in the same patient (6 patients) during painful and painless myocardial ischemia. The echocardiographic changes observed during silent ischemic attacks were significantly different from those detected during symptomatic attacks. The latter were characterized by a larger extension of the ischemic myocardium and, as a consequence, by a larger functional impairment. Symptomatic and asymptomatic ischemic attacks were recorded echocardiographically in the same patient during repeated attacks on the same day, and were always clearly differentiated by the degree of wall motion abnormalities. The echocardiographic monitoring during the ischemic attack seemed to confirm that the greater functional impairment preceded the onset of pain leading to the occurrence of this symptom. Nevertheless, it was impossible to identify a threshold value above which the ischemic attack will be symptomatic. Our data seem to indicate a close relationship between painful ischemia and a higher degree of ischemic damage. Thus, in patients with predominantly painful myocardial ischemia, the extension and the severity of ischemia could play an important role in determining this symptom.

The feasibility of echocardiography in detecting left ventricle wall motion abnormalities, their location and their spontaneous or therapeutic regression, was assessed performing monodimensional and two-dimensional echocardiography in 35 patients with stable effort angina, without previous AMI. A control group of 10 normal subjects was also studied. The Authors evaluated echocardiographic findings on subjects at rest, during supine bicycle exercise and after sublingual nitroglycerin administration, defining the quality of wall motion as normal, hypokinetic, akinetic or dyskinetic in M-mode, and normal or asynergic in 2-D. They also analyzed, in M-mode, some echocardiographic indices of regional left ventricle function (IVSE, PWE, VIVS, VPW, delta TS, delta TP), and, in 2-D, the percent of systo-diastolic endocardial outline changes versus standard references in 7 sectors of left ventricle (anterior, lateral, inferior, septal in short-axis, septal, postero-lateral in long-axis, and apical) by means of a HP 9845B Computer, interfaced to a Digitizer. The percentage of feasibility of exercise echocardiography has been 60% in M-Mode, and 70% in 2-D. Mono and two-dimensional findings were normal in all patients at rest, whereas, during exercise, 57% of them, in M-mode, and 88% in 2-D, showed segmental contraction abnormalities. The Authors conclude that exercise echocardiography, though technically difficult, is feasible, Both M-mode and 2-D involve peculiar advantages or disadvantages. They provide, however, a valuable tool in detecting the mechanical consequences of exercise-induced regional myocardial ischemia and may be applicable in patients with equivocal exercise test.