Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling.

OBJECTIVES: The purpose of this study was to determine whether contractile recovery induced by dobutamine in dysfunctioning viable myocardium supplied by nearly occluded vessels is related to an increase in blood flow in the absence of collaterals. BACKGROUND: Dobutamine is used to improve contractility in ventricular dysfunction during acute myocardial infarction. However, it is unclear whether a significant increase in regional blood flow may be involved in dobutamine effect. METHODS: Twenty patients with 5- to 10-day old anterior infarction and > or =90% left anterior descending coronary artery stenosis underwent 99mTc-Sestamibi tomography (to assess myocardial perfusion) at rest and during low dose (5 to 10 microg/kg/min) dobutamine echocardiography. Rest echocardiography and scintigraphy were repeated >1 month after revascularization. Nine patients had collaterals to the infarcted territory (group A), and 11 did not (group B). RESULTS: Baseline wall motion score was similar in both groups (score 15.9+/-1.3 vs. 17.4+/-2.0, p = NS), whereas significant changes at dobutamine and postrevascularization studies were detected (F[2,30] = 409.79, p < 0.0001). Wall motion score improved significantly (p < 0.001) in group A both at dobutamine (-5.3+/-2.2) and at postrevascularization study (-5.5+/-1.9), as well as in group B (-3.9+/-2.8 and -4.5+/-2.4, respectively). Baseline 99mTc-Sestamibi uptake was similar in both groups (62.9+/-9.7% vs. 60.3+/-10.4%, p = NS), whereas at dobutamine and postrevascularization studies a significant change (F[2,30] = 65.17, p < 0.0001) and interaction between the two groups (F[2,30] = 33.14, p < 0.0001) were present. Tracer uptake increased significantly in group A both at dobutamine (+ 10.9+/-7.9%, p < 0.001) and at postrevascularization study (12.1+/-8.7%, p < 0.001). Conversely, group B patients showed no change in tracer uptake after dobutamine test (-0.4+/-5.8, p = NS), but only after revascularization (+8.8+/-7.2%, p < 0.001). CONCLUSIONS: The increase in contractility induced by low dose dobutamine infusion in dysfunctional viable myocardium supplied by nearly occluded vessels occurs even in the absence of a significant increase in blood flow.

Handgrip increases endothelin-1 secretion in normotensive young male offspring of hypertensive parents.

OBJECTIVES: We tested the hypothesis that an abnormal response of plasma endothelin-1 (ET-1) is elicited by handgrip exercise (HG) in young normotensive offspring of hypertensive parents. BACKGROUND: It has been hypothesized that ET-1 is involved in blood pressure control and plays a pathophysiologic role in the development of clinical hypertension. METHODS: Two groups of healthy male subjects, 11 with hypertensive parents (group A) and 10 without a family history of hypertension (group B), underwent 4 min of HG at 50% maximal capacity. Heart rate and blood pressure and plasma levels of ET-1, epinephrine and norepinephrine were measured at baseline, peak HG, and after 2 (R2) and 10 (R10) min of recovery. RESULTS: Group A had higher norepinephrine levels than group B throughout the test (baseline 181+/-32 [SEM] vs. 96+/-12 pg/ml, p < 0.05; peak HG 467+/-45 vs. 158+/-12 pg/ml, p < 0.000001; R2 293+/-46 vs. 134+/-8 pg/ml, p < 0.01; RO1 214+/-27 vs. 129+/-10 pg/ml, p < 0.0005); no significant difference in epinephrine levels was detected. Compared with group B subjects, group A had higher baseline ET-1 levels (1.07+/-0.14 vs. 0.59+/-0.11 pg/ml, p < 0.02), which increased to a greater extent at peak HG (1.88+/-0.31 vs. 0.76+/-0.09 pg/ml, p < 0.005) and R2 (2.46+/-0.57 vs. 1.31+/-0.23 pg/ml, p < 0.05) and remained elevated at R10 (3.16+/-0.78 vs. 0.52+/-0.09 pg/ml, p < 0.002). Multivariate analysis demonstrated that only a family history of hypertension (chi-square=7.59, p=0.0059) and ET-1 changes during HG (chi-square=4.23, p=0.0398) were predictive of blood pressure response to HG and that epinephrine and norepinephrine were not. CONCLUSIONS: The response to HG in offspring of hypertensive parents produced increased ET-1 plasma levels and resulted in a sustained ET-1 release into the bloodstream during recovery compared with offspring of normotensive parents. This may be an important marker for future clinical hypertension.

Interleukins 6 and 8 as mediators of acute phase response in acute myocardial infarction.

The present study provides evidence that interleukin (IL)-6 and IL-8 are the main endogenous mediators of acute phase response in patients with myocardial infarction. This conclusion was supported by the observation of a strict relation between IL-6 elevation and the extent of myocardial tissue damage and rise in body temperature.

Isometric handgrip exercise increases endothelin-1 plasma levels in patients with chronic congestive heart failure.

This study demonstrated an immediate and short-lasting endothelin-1 release in the circulation of patients with severe chronic congestive heart failure during isometric handgrip exercise, but not in normal subjects. Our data suggest that endothelin-1 levels may increase transiently during daily physical activity, thus contributing to progressive deterioration of left ventricular function.

Enoximone coupled to very low dose dobutamine echocardiography detects myocardial viability in akinetic and dyskinetic post-myocardial infarcted areas.

Dobutamine and enoximone stimulate independently inotropic reserve by increasing intracellular cyclic adenosine monophosphate. The potential of enoximone (0.75 mg/kg body weight over 10 minutes) followed by very low dose (2.5 microg/kg/min) dobutamine echocardiography to predict recovery of ventricular function in akinetic and dyskinetic postinfarcted areas was studied. We enrolled 22 patients with previous Q-wave myocardial infarction and regional wall motion abnormalities related to left anterior descending arterial disease, left ventricular ejection fraction <40%, and all scheduled for myocardial revascularization. A 10 microg/kg/min dobutamine test was performed 48 hours before the study protocol. Test images obtained at peak of pharmacodynamic effects were compared with those obtained at 4 months after myocardial revascularization. We used a 16-segment ventricular model and a 5-grade scoring system. Resting regional myocardial dysfunction graded > or =2 was present in 267 of 352 segments evaluated. Contractile reserve (decrease in resting wall motion score > or =2 grades) at peak effect of enoximone infusion was present in 34 of 112 severely hypokinetic, 42 of 117 akinetic, and 14 of 38 dyskinetic segments. The inotropic reserve evaluated after very low dose dobutamine was observed in 34 of 112 severely hypokinetic, 49 of 117 akinetic, and 20 of 38 dyskinetic segments. After revascularization, recovery of function was observed in 31 of 112 severely hypokinetic, 49 of 117 akinetic, and 21 of 38 dyskinetic segments. Overall, there was a significant correlation between absolute score changes of segments which were abnormal at baseline (n = 267) to enoximone peak effects (r = 0.49, p <0.001) to predict absolute changes after revascularization; after dobutamine there was progress toward identity (r = 0.62, p <0.001) and the difference was significant among correlation slopes of dobutamine alone, enoximone alone, and enoximone plus very low dose dobutamine echocardiograophy (0.45+/-0.04, 0.51+/-0.04, and 0.63+/-0.04, respectively, F = 5.25, p = 0.005). Therefore, enoximone followed by very low dose dobutamine may assess myocardial viability of postinfarcted akinetic and dyskinetic areas. This test may be useful when evaluating patients with more severe cardiac failure and/or life-threatening arrhythmias.

Pretreatment with the adenosine triphosphate-sensitive potassium channel opener nicorandil and improved myocardial protection during high-potassium cardioplegic hypoxia.

We hypothesized that pretreatment with the potassium channel opener nicorandil might enhance myocardial protection achieved by cold (20 degrees C) high-potassium (16 mmol/L) cardioplegia (5 ml/min) during long-duration (120 minutes) myocardial hypoxia (average oxygen content 5.4 ml/dl). We tested a 15-minute infusion of nicorandil (1 mmol/L) given only before (group A, n = 8) or before and during cardioplegia (group B, n = 8) in guinea pig papillary muscle preparations contracting isometrically while stimulated (4 mA, 2 msec) at 1600 msec cycle length. Nicorandil was significantly negative inotropic before cardioplegia and shortened significantly action potential duration. During cardioplegia, time to arrest of contraction was shortened from 145 +/- 28 seconds (mean +/- standard error) in the vehicle group (dimethyl sulfoxide 1:100; n = 8) to 56 +/- 10 seconds (p < 0.02) and 68 +/- 5 seconds (p < 0.05) in groups A and B, respectively. Recovery of developed tension at 60 minutes of normothermic reoxygenation (expressed as percent of prehypoxia basal value) was ameliorated from 54% +/- 6% (vehicle group) to 92% +/- 4% (group A, p < 0.01) and to 119% +/- 19% (group B, p < 0.01). The specific potassium channel blocker glibenclamide (glib: 1 mumol/L, n = 8) prolonged action potential duration and was without effect on time to arrest. On reoxygenation, the glib group had prolonged time to half relaxation (versus group A, p < 0.02) and the worst percent developed tension at 60 minutes (40% +/- 4%). In the overall study, time to arrest and percent developed tension at 60 minutes were inversely correlated (r = -0.45, p < 0.01). Arrhythmias were never observed. Multivariate analysis showed that pretreatment with nicorandil (with or without drug adjunct to cardioplegic solution) was a significant factor (r2 = 0.65, p = 0.0001) to influence reoxygenation-mediated recovery of mechanical function. Neither the negative inotropic effect of nicorandil before cardioplegia nor its abbreviating action on time to arrest during cardioplegia was contributory to explain recovery of function on reoxygenation. In subgroup analysis, negative inotropism and the shortening of action potential duration were contributory factors. These data suggest that nicorandil pretreatment activates potassium channels and enhances the myocardial protection provided by cold cardioplegia an effect, which is evident after a long hypoxic period, late on reoxygenation.

Adenosine triphosphate-dependent potassium channel modulation and cardioplegia-induced protection of human atrial muscle in an in vitro model of myocardial stunning.

OBJECTIVES: Although adenosine triphosphate-dependent potassium channel openers have been shown to enhance cardioplegic protection in animal myocardium, there is a lack of data on human cardiac tissues. We aimed at determining, on human atrial muscle, whether adenosine triphosphate- dependent potassium channels are involved in protection caused by high-potassium cardioplegia and whether adenosine triphosphate-dependent potassium channel activation might improve cardioplegic protection in an in vitro model of myocardial stunning. METHODS: Human atrial trabeculae were obtained from adult patients undergoing cardiac operations. In an organ bath at 37 degrees C, the preparations were subjected to 60 minutes of hypoxia at a high stimulation rate either in Tyrode solution (control, n = 17) or in St Thomas' Hospital solution without additives (n = 6) or associated with 100 nmol/L bimakalim (n = 7) or 1 micromol/L glibenclamide (n = 7), followed by 60 minutes of reoxygenation and 15 minutes of positive inotropic stimulation with 1 micromol/L dobutamine. RESULTS: Atrial developed tension was reduced by hypoxia to 27% +/- 5% of baseline and incompletely recovered after reoxygenation to 38% +/- 7%, whereas dobutamine restored contractility to 74% +/- 7% of basal values. St Thomas' Hospital solution with or without bimakalim improved developed tension after reoxygenation and dobutamine (P <.0001 vs control), whereas glibenclamide inhibited these protective effects of cardioplegic arrest (P =.001 vs St Thomas' Hospital solution). After reoxygenation, the protective effect of bimakalim disappeared at a high pacing rate (400- and 300-ms cycle length) but recovered during dobutamine superfusion. CONCLUSIONS: Adenosine triphosphate-dependent potassium channels are likely involved in the cardioprotective effects of cardioplegia in human atrial trabeculae and adenosine triphosphate-dependent potassium channel activation with bimakalim used as an additive to cardioplegia enhanced protection.

Cicletanine prevents the excitation-conduction blocks induced by terfenadine in ischemic myocardium.

Terfenadine, a histamine H(1) receptor antagonist, has been associated with clinical ventricular arrhythmias and in vitro excitation-conduction blocks, whereas anti-ischemic and antiarrhythmic effects have been shown with cicletanine, a prostacyclin generation stimulator. We aimed at determining in vitro if cicletanine can protect the ischemic myocardium from excitation-conduction blocks and specifically those induced by terfenadine. In a double-chamber bath, isolated guinea pig ventricular strips were partly exposed to normoxia and partly to ischemic, then reperfused, conditions, in the presence of 10 microM terfenadine, 10 microM indomethacin (prostacyclin generation blocker) or the solvent (dimethylsulfoxide 1:100, control) randomly allocated, and thus either in the absence (n=20) or presence (n=21) of 10 microM cicletanine during the total protocol duration. The multivariate Cox's model was used to predict the excitation-conduction block events and to assess the estimated survival of preparations (excitation-conduction block-free rate). Cicletanine protected the preparations (relative risk=0.08, t=-3.28) from the ischemia-induced excitation-conduction blocks (estimated survival=0.83 versus 0.30 in control), and this effect was abolished by indomethacin (estimated survival=0.35). Terfenadine enhanced 3. 58-fold the risk of occurrence of excitation-conduction blocks during ischemia (t=2.10) and this effect was inhibited by cicletanine pretreatment (estimated survival=0.40 versus 0.10 in untreated preparations). In conclusion, these in vitro findings have provided evidence for (1) protective effects of cicletanine against ischemia-induced excitation-conduction blocks, possibly related to its stimulating activity on local prostacyclin generation, and (2) efficacy of cicletanine to prevent excitation-conduction blocks induced by terfenadine in ischemic cardiac tissue.

Nitroglycerin-induced changes in myocardial sestamibi uptake to detect tissue viability: radionuclide comparison before and after revascularization.

BACKGROUND: Nitroglycerin (NTG) is known to increase the blood supply to the myocardium, and would thus increase the delivery of a perfusional tracer such as sestamibi (MIBI) to the tissue. The latter, in turn, would take up and concentrate the tracer to a greater extent than in basal conditions only if energy-dependent mechanisms were still available-that is, only if the cells were still viable. METHODS: We evaluated the changes that intravenous administration of NTG induced on the uptake of MIBI by akinetic myocardial areas, using tomographic perfusional imaging in 23 patients with previously ascertained anterior myocardial infarction who were undergoing myocardial revascularization procedures. Changes in uptake were compared with echocardiographic and perfusional changes occurring after operation. RESULTS: The improvement of MIBI uptake after NTG correctly identified 12 of the 16 patients (75%) showing postoperative wall motion improvement; they comprised 12 of the 14 (86%) patients with NTG-induced increase in MIBI uptake who showed improved wall motion after operation. A close correlation (r = 0.88, P < 0.001) was found between the increase in myocardial MIBI uptake induced by NTG infusion and that induced by revascularization. The presence of collaterals to the akinetic area was associated with a significantly (P < 0.01) greater increase in MIBI uptake both during NTG infusion and after operation. CONCLUSIONS: The results of this study suggest that MIBI perfusional myocardial scintigraphy during infusion of NTG is capable of detecting viable but chronically hypoperfused myocardium, predicting postoperative wall motion and perfusional improvement, and reflecting the postoperative pattern of perfusion. The best results were achieved in patients with evidence of collateral circulation supplying the infarcted area.

Dynamic exercise induces elevation of plasma levels of endothelin-1 in patients with coronary artery disease.

In this investigation the response of endothelin-1 plasma levels to dynamic exercise in patients with coronary artery disease (CAD) was studied. The study population consisted of 20 patients with CAD, 16 men and 4 women (mean age 53 +/- 8.6 years). Seven normal volunteers all men (mean age 53.4 +/- 4.4 years) were studied as a control group. Seven patients had prior myocardial infarction. All patients and controls exercised on a multi-stage bicycle ergometer; plasma endothelin-1 levels and hemodynamic indices were measured at rest, at peak exercise, and at two and six minutes after exercise. Of the 20 patients examined, 7 (35%) showed electrocardiogrpahic (ECG) signs of myocardial ischemia during the stress test. The mean plasma endothelin-1 concentration increased significantly from 7.8 +/- 3.0 to 13.6 +/- 3.5 pg/mL at exercise peak (P < 0.05) only in patients who did not show ECG signs of myocardial ischemia and returned to baseline values during recovery (six minutes) (9.4 +/- 2.1 pg/mL). In normal subjects baseline endothelin-1 levels (9.4 +/- 4.2 pg/mL) were not significantly altered at peak exercise (10.8 +/- 4.7 pg/mL) and at recovery (11.3 +/- 3.6 pg/mL). The hemodynamic parameters were not correlated with the plasma endothelin-1 levels before, during, and after exercise in all groups. The present study demonstrated that the plasma levels of endothelin-1 in patients with CAD increased significantly during stress testing.

Plasma endothelin-1 concentrations in patients with coronary artery disease during stress test before and after nisoldipine administration.

The purpose of this study was to determine the response of plasma levels of endothelin-1 (ET-1) to dynamic exercise in patients with coronary artery disease and chronic stable angina pectoris and positive exercise tolerance test, before and after treatment with the calcium antagonist nisoldipine (20 mg/day buccally for 7 days). Plasma ET-1 levels and hemodynamic parameters (blood pressure and heart rate) were determined at rest, at peak exercise and recovery. All patients had a positive electrically and clinically stress test and all of the eight patients did not developed ECG signs of myocardial ischemia after nisoldipine administration. Before nisoldipine treatment the plasma ET-1 levels did not increase significantly during exercise. After nisoldipine treatment the plasma ET-1 levels were significantly lower at rest and during exercise compared with those revealed before calcium antagonist treatment. In conclusion our results suggest that in patients with chronic stable angina pectoris the treatment with calcium antagonist nisoldipine reduced ischemia and plasma ET-1 levels.

beta-Endorphin and propiomelanocortin-correlates peptides response in suspected and confirmed ischemic heart disease during exercise.

UNLABELLED: In this study, we investigated circulating beta-endorphin, ACTH and cortisol in subjects with suspected coronary artery disease (CAD) and in patients with CAD during stress testing. Group I: 18 subjects, all male (average age 48 +/- 9 yrs) with suspected (CAD) were enrolled. Group II: 35 patients, 30 males and 5 females (average age 54.3 +/- 7 yrs) with CAD, were enrolled. Ten patients had previous myocardial infarction. In all patients that underwent coronarography a stenosis > 75% was found in at least one coronary artery. The stress test was performed with a cycloergometer, increasing work loads 25 watt every 2 min. All subjects and patients were in the recumbent position for at least 30 minutes prior to testing. During this period a 3-way catheter was placed in the antecubital vein and blood was drawn for Beta-endorphin, ACTH and cortisol; additional blood samples were drawn using a pre-chilled syringe at maximum effort and during the recovery period. RESULTS: group I: 9 of the subjects with suspected CAD had either ECG or clinical signs of ischemic during the stress test. In subjects with a negative test, the test was carried out for a longer period of time and at a higher work load. There was an increase in Beta-endorphin and ACTH at peak exercise and during recovery. Plasma cortisol increase during the period of recovery. Group II: 16 of the 35 patients with CAD exhibited ECG signs of induced myocardial ischemia; there was no difference in work loads in patients with positive or negative stress test. Exercise time was reduced in all patients and plasma Beta-endorphin increased at peak exercise and recovery in patients with a negative stress test. In conclusion our study revealed a different response of Beta-endorphin, ACTH and cortisol plasma levels in subjects with suspected CAD and in patients with CAD during exercise testing.

[Influence of antihypertensive therapy on the "white coat effect"]. / Influenza della terapia antipertensiva sull "effetto camice".

The aim of this study was to evaluate the alarm reaction when hypertensive patients either receiving or not receiving drug therapy have their blood pressure measured (the so-called "White coat effect"). A group of 64 patients (38 males and 26 females, mean age 52 +/- 11 years, OMS stage I-II) was studied. Twenty-three patients were not receiving antihypertensive therapy, 41 patients were regularly taking antihypertensive therapy prescribed by their own doctors. Non-invasive monitoring of arterial pressure (AP) and heart rate (HR) was carried out in all patients. The following parameters were examined in this study: mean of 3 measurements of AP and HR before monitoring (CAP, CHR), daily mean of AP and HR monitoring (MAP, MHR). The following results were obtained: 1) non-treated patients, CAP 157/108 +/- 19/11 mmHg, CHR 83 +/- 11 b/min, MAP 155/100 +/- 20/7 mmHg, MHR 76 +/- 7 b/min; 2) treated patients, CAP 151/96 +/- 21/16 mmHg, CHR 73 +/- 16 b/min, MAP 142/86 +/- 15/12 mmHg, MHR 70 +/- 10 b/min. The two-tailed "t"-test for paired data showed a statistically significant difference (p < 0.001) between diastolic CAP and diastolic MAP in both groups of patients. Systolic CAP was significantly greater than systolic MAP in treated patients (p < 0.01), whereas CHR was significantly higher than MHR in non-treated patients (p < 0.001). These data demonstrate that the alarm reaction to measuring blood pressure is present in both treated and non-treated hypertensive patients. Antihypertensive treatment appears to lessen the chronotropic but not the pressure response to measurement of AP in a hospital setting.

Cardiovascular reactions to physiological stimuli in the elderly and the relationship with the autonomic nervous system.

In order to evaluate age-related differences in autonomic nervous system control of the cardiovascular system, we studied two groups of healthy subjects of different ages by means of an autonomic function test, the posture test, applied before and after meals. Our results suggest that the reactions of the cardiovascular system to physiological stimuli such as meals or standing up, differ in elderly compared with young people, partly because age modifies the balance between the parasympathetic and the orthosympathetic nervous systems. In the elderly there is a progressive decline in parasympathetic function, which controls the initial heart rate response to standing up. Splanchnic blood pooling and possible hormonal secretions after meals may produce a drop in blood pressure due to cardiovascular modifications in the elderly. Other factors contributing to the different patterns found in the elderly may be reduced compliance of the vascular tree, a decreased baroreceptor response and decreased sympathetic activity.

[Natural harmonic echocardiography]. / Ecocardiografia in armonica naturale.

The acquisition of echocardiographic images in harmonic mode (a frequency double than the transmitted, or fundamental) improves imaging quality. We assessed whether harmonic imaging improves the detection of endocardial borders, evaluation of ventricular function and diagnostic confidence in the clinical arena. We have studied in fundamental and harmonic imaging 45 patients (age 20-89 years, mean 53 years) using a multifrequency transthoracic probe transmitting at 1.75 MHz and receiving at 3.5 MHz (Acuson Sequoia). In 34 low echogenic patients we assessed left ventricular function. The remaining 11 patients represented selected cases (i.e. atrial septal aneurysm, aortic dissection, endocarditis and atrial septal defect). The echocardiographic images were recorded on a magneto-optical disk and analyzed by two blinded observers. Endocardial definition has been semiquantitatively evaluated assigning a 0-4 score for each of the 16 segments of the left ventricle. A score of 0 was allotted to the non-visualizable segments and a score of 4 to the best detectable segments. Ejection fraction was calculated in each patient from the apical 4-chamber view. We compared endocardial border definition and ejection fraction at rest, in fundamental and harmonic mode, and assessed the interobserver agreement in the calculation of ejection fraction. Harmonic images always showed a better definition and lower noise compared to fundamental. Endocardial border definition was significantly improved in all segments (from 1.3 +/- 1.1 fundamental to 2.9 +/- 1.0 harmonic). Forty-two segments were non detectable in fundamental (score 0) compared to 5 in harmonic. Of these 42 segments, 37 were detectable in harmonic, with a score of 2.0 +/- 1.0. Conversely, none of the 5 segments non detectable in harmonic could be visualized in fundamental. The interobserver agreement in calculating ejection fraction was improved by harmonic imaging compared to fundamental (r = 0.91 and r = 0.67, respectively). In the selected clinical cases the diagnosis was easier and faster by harmonic imaging. The harmonic mode drastically improves echocardiographic imaging, it may be used routinely and reduce the need for more invasive techniques such as transesophageal echocardiography.

[The correlation between left ventricular segmental kinesis and a Selvester QRS analysis in stabilized myocardial infarct]. / Correlazione tra alterazioni della cinesi segmentale ventricolare sinistra e analisi del QRS secondo Selvester nell'infarto miocardico stabilizzato.

We have studied the relationship between left ventricular segmental wall motion evaluated by means of biplane left ventricular cineangiography and the myocardial infarct size estimated using Selvester's scoring system based on the QRS of the electrocardiogram. Seventy consecutive patients with old myocardial infarction were recruited. All patients underwent diagnostic retrograde left heart catheterization including left ventriculography and selective coronary arteriography. Nineteen patients were excluded from the study due to intraventricular conduction disturbances and left ventricular hypertrophy. Of the remaining 51 patients, aged 33-76 years (mean 56 years), 31 had inferior or postero-inferior myocardial infarction (Group 1); 7 patients had combined anterior and inferior myocardial infarction (Group 2); 13 patients had anterior or antero-septal myocardial infarction (Group 3). The analysis of left ventricular segmental wall motion was performed according to the Collaborative Studies in Coronary Artery Surgery assigning at hypokinesia, akinesia and dyskinesia 1, 2 and 3 points, respectively. The values of statistical correlations between QRS scoring system and ventricular scoring were: r = 0.85 (Group 1); r = 0.78 (Group 2); r = 0.70 (Group 3). Our data indicate that Selvester's scoring system may provide useful information on functional status and on the extent of left ventricular wall motion abnormalities in patients with previous myocardial infarction.