Biomedical subjects

P L Temporelli

Publications and source records attributed to P L Temporelli.

31 records · Page 2Linked to original sources

PubMed1996

[Exertion-induced myocardial ischemia has little influence on ventricular remodeling in post-infarction patients with preserved systolic function].

BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well documented. However, the role of residual exertional ischemia in the remodelling process after infarction has not yet been established. In this study, we investigated whether exercise-induced myocardial ischemia influences left ventricular remodelling in patients with recent myocardial infarction and preserved left ventricular function and volumes. METHODS: Sixty-four patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy; the echocardiographic examination at rest was repeated 6 months later. Based on the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were classified as having no exertional ischemia (group 1, n = 13 [20%]), mild to moderate ischemia (group 2, n = 32 [50%]) and severe exertional ischemia (group 3, n = 19 [30%]). RESULTS: At 5 weeks after infarction left ventricular volumes, ejection fraction, percent wall motion abnormalities and regional dilatation were similar in the three groups. After 6 months, end-diastolic and end-systolic volumes and regional dilatation did not change in patients in all groups, while ejection fraction and percent wall motion abnormalities showed a slight but significant (p < 0.01) improvement in all groups. CONCLUSIONS: Exercise-induced myocardial ischemia, either mild or severe, does not affect ventricular remodelling and function after myocardial infarction in patients with preserved ejection fraction.

Adult↗

PubMed1996

[A paradigmatic case of partial agenesis of the pericardium].

Complete or partial absence of the pericardium is an uncommon congenital abnormality. Since its first description, several cases have been reported. Although the clinical and instrumental features of this defect are well described, at present it is often overlooked. We report a case of a 19-year old boy referred to our Echocardiography laboratory because of a suspected interatrial septal defect. For this reason it has been recommended to undergo cardiac catheterization. The patient, completely asymptomatic, had a negative physical examination. The echocardiogram excluded the presence of an interatrial septal defect, but some abnormalities, regarding overall right-sided heart, were found (paradoxical interventricular septal movement, apparent right-sided heart enlargement, with unusual bulging of the apex of the right ventricle, an excessive basculant heart movement). In the absence of any other heart disease, we thought that these abnormalities reflected a congenital absence of the pericardium. Indeed, the chest X-ray showed some features, considered patognomonic for congenital absence of the pericardium (levoposition of the heart, lung interposition between the diaphragm and the base of the heart and between the aorta and pulmonary artery). Nuclear magnetic resonance study showed the absence of the pericardium in the posterior and posterolateral wall, confirming our suspicion. Furthermore, the posterior wall of the heart leaned to herniate through the pericardial defect. Since the partial absence of the pericardium can lead to severe complications, surgery was recommended. The correct diagnosis of this disease is very important because of its prognostic implications; this case represents a further contribution to the understanding of this defect.

Adult↗

PubMed1995

Technetium-99m sestamibi tomographic evaluation of residual ischemia after anterior myocardial infarction.

OBJECTIVES: This study investigated the value of sestamibi scintigraphy in assessing residual ischemia after anterior myocardial infarction. BACKGROUND: Serial imaging with sestamibi, the uptake and retention of which correlate with regional myocardial blood flow and viability, has been used to estimate salvaged myocardium and risk area after acute infarction. We recently documented that recovery of perfusion and contraction in the infarcted area may continue well after the subacute phase, suggesting myocardial hibernation. Some underestimation of viability in the setting of hibernating myocardium by sestamibi imaging has been reported. METHODS: We studied 58 patients in stable condition after Q wave anterior infarction. Regional perfusion and function were quantitatively assessed by sestamibi tomography and two-dimensional echocardiography at 4 to 6 weeks and at 7 months after infarction. In sestamibi polar maps, abnormal areas with tracer uptake > 2.5 SD below our reference values were computed at rest and after symptom-limited exercise. On two-dimensional echocardiography the ejection fraction and extent of rest wall motion abnormalities were assessed by a computerized system. All patients had coronary angiography between the two studies. RESULTS: At 7 months the extent of rest sestamibi defect was significantly reduced in 40 patients (69%, group 1) and unchanged in 18 (31%, group 2). Rest wall motion abnormalities and ventricular ejection fraction significantly improved in group 1 but not in group 2. Underlying coronary disease, patency of the infarct-related vessel and rest sestamibi defect extent at 5 weeks were comparable between the two groups. At 7 months, an increase in the reversible (stress-rest defect) tracer defect was observed in group 1 (p < 0.05) despite a smaller stress-induced hypoperfusion (p < 0.05). Reversible sestamibi defects and stress hypoperfusion were unchanged in group 2. In 38 (95%) of 40 group 1 patients, the area showing reversible sestamibi defects at 7 months matched the area showing fixed hypoperfusion at 5 weeks. CONCLUSIONS: The reduction in the rest tracer uptake defect that can occur late after infarction may affect the assessment of ischemic burden by sestamibi imaging early after anterior myocardial infarction.

Adult↗

PubMed1995

Residual exertional ischemia and unfavorable left ventricular remodeling in patients with systolic dysfunction after anterior myocardial infarction.

OBJECTIVES: This study investigated whether exercise-induced myocardial ischemia influences left ventricular remodeling after anterior myocardial infarction. BACKGROUND: The effects of acute and recurrent ischemia on ventricular function are well established. However, to our knowledge the role of exertional ischemia in the remodeling response after infarction has not been investigated. METHODS: Ninety-one patients with a first anterior Q wave myocardial infarction were studied at 5 weeks by rest echocardiography and exercise scintigraphy. The echocardiographic examination was repeated 6 months later. On the basis of the presence and extent of reversible perfusion defects on exercise scintigraphy, patients were assigned to groups with no exertional ischemia (group 1, n = 20 [22%], mild to moderate ischemia (group 2, n = 45 [49%]) and severe exertional ischemia (group 3, n = 26 [29%]). RESULTS: Initial left ventricular volumes were similar, and no differences were found among the three groups in the remodeling response over the 6-month period of the study. However, patients in groups 2 and 3 with an ejection fraction < or = 40% showed significant (p < 0.01) ventricular enlargement over time, which was similar between the two groups (end-diastolic volume [mean +/- SD] from 74 +/- 13 to 80 +/- 17 ml/m2 in group 2 and from 72 +/- 11 to 81 +/- 19 ml/m2 in group 3; regional dilation from 42 +/- 16% to 52 +/- 22% in group 2 and from 38 +/- 18% to 46 +/- 27% in group 3). In contrast, ventricular dimensions did not change in group 1 patients with an ejection fraction < or = 40% as well as in patients in all three groups with an ejection fraction > 40%. CONCLUSIONS: Exercise-induced myocardial ischemia may contribute to progressive ventricular enlargement in patients with poor left ventricular function after a large anterior myocardial infarction.

Analysis of Variance↗

PubMed1995

[Estimate of lung capillary pressure and identification of the "pseudonormal" transmitral flow pattern in patients with severe systolic dysfunction of the left ventricle].

OBJECTIVES: Aim of this study was to investigate whether Doppler-derived transmitral flow velocity variables would allow a reliable estimate of pulmonary capillary wedge pressure in patients with left ventricular systolic dysfunction and normal mitral flow velocity pattern, and would then predict the presence of a "pseudonormal" transmitral flow velocity profile. BACKGROUND: Abnormal relaxation and increased chamber stiffness have opposing effects on the left ventricular filling pattern. When both abnormalities are present at the same time, as often occurs in patients with systolic dysfunction, the mitral pattern may appear to be normal: in this case the ability of Doppler recording to assess diastolic function and predict left ventricular filling pressure may be significantly compromised. METHOD: Pulmonary capillary wedge pressure (PWP) and Doppler transmitral flow velocity profile were simultaneously recorded in 70 postinfarction patients with ejection fraction < or = 35% and mitral flow velocity pattern apparently normal (E/A ratio between 1 and 2). Doppler traces were analyzed using a microcomputer-based digitizing system, and the following variables were measured: peak flow velocity in early diastole (E) and during atrial contraction (A), peak E/A wave velocity ratio and the deceleration time (Dec T) of early diastolic flow. RESULTS: Mean E/A ratio was 1.3 +/- 0.2 and mean PWP was 17 +/- 7 mm Hg. Forty-two patients had a PWP < 20 mm Hg and the remaining 28 patients (40%) had PWP > or = 20 mm Hg. Peak E, peak A and E/A ratio were similar in the two groups, whereas Dec T was significantly (p < 0.001) lower in patients with > or = 20 mm Hg PWP (93 +/- 15 vs 146 +/- 19 msec). A very weak correlation was found between PWP and both E and A velocity (r = 0.14 and r = 0.09, respectively). Furthermore, no correlation was found between E/A ratio and PWP (r = 0.08). Conversely, a very close negative correlation was observed between Dec T of early filling and PWP (r = -0.96). Sensitivity and specificity of < or = 120 ms in Dec T in predicting > or = 20 mm Hg in PWP were 100% and 99%, respectively. CONCLUSIONS: These data point out the relevant role of Doppler-derived deceleration time of early diastole in predicting left ventricular filling pressure. In patients with left ventricular systolic dysfunction an apparently normal diastolic filling pattern is often associated with elevated PWP. Through the estimate of increased PWP, early deceleration time seems to provide an important means of differentiating a real normal from a pseudonormal or masked abnormal filling pattern caused by increased left ventricular filling pressure.

Adult↗

PubMed1994

Doppler-derived mitral deceleration time of early filling as a strong predictor of pulmonary capillary wedge pressure in postinfarction patients with left ventricular systolic dysfunction.

OBJECTIVES: The aim of this study was to investigate the correlations between Doppler-derived transmitral flow velocity variables and pulmonary capillary wedge pressure in patients with severe left ventricular systolic dysfunction. BACKGROUND: Abnormal relaxation and increased chamber stiffness have opposing effects on the left ventricular filling pattern. When both abnormalities are present at the same time, as often occurs in patients with systolic dysfunction, the ability of Doppler recording to assess diastolic function and predict left ventricular filling pressure may be significantly compromised. METHOD: Pulmonary capillary wedge pressure and Doppler transmitral flow velocity profile were simultaneously recorded in 140 postinfarction patients with ejection fraction < or = 35%. RESULTS: Correlation between the ratio of mitral peak flow velocity in early diastole to peak flow velocity in late diastole (E/A ratio) and pulmonary capillary wedge pressure was weak (r = 0.65). Although the specificity of E/A > or = 2 in predicting > or = 20 mm Hg in pulmonary capillary wedge pressure was high (99%), its sensitivity was low (43%). Conversely, a very close negative correlation was found between mitral deceleration time of early filling and pulmonary capillary wedge pressure (r = -0.90). Sensitivity and specificity of < or = 120 ms in deceleration time in predicting > or = 20 mm Hg in pulmonary capillary wedge pressure were 100% and 99%, respectively. CONCLUSIONS: Doppler-derived mitral deceleration time of early filling provides a simple and accurate means of estimating pulmonary capillary wedge pressure that is particularly useful in patients with a normal or normalized mitral flow velocity pattern.

Adult↗

PubMed1994

Spontaneous delayed recovery of perfusion and contraction after the first 5 weeks after anterior infarction. Evidence for the presence of hibernating myocardium in the infarcted area.

BACKGROUND: In patients with ventricular dysfunction caused by stunning or hibernation, it is not clear when complete recovery of the salvaged myocardium occurs after acute myocardial infarction. The purpose of this study was to determine whether a delayed recovery of perfusion and contraction continues even after the subacute phase. METHODS AND RESULTS: We prospectively studied 71 consecutive male patients with first uncomplicated Q-wave anterior infarction. Resting regional blood flow distribution and contraction were assessed quantitatively 5 weeks and 7 months after the acute phase by serial sestamibi tomography and two-dimensional echocardiography. Coronary angiography also was performed in 52 patients. Overall, at 7 months there was an improvement in the perfusion defect severity (1019 +/- 811 versus 1365 +/- 821 at 5 weeks, P < .001) as well as in the extent of abnormal wall motion (28 +/- 19% versus 32 +/- 15%, P < .001) and left ventricular ejection fraction (53 +/- 14% versus 50 +/- 13%, P < .01). Among the 68 of 71 patients showing resting perfusion defects at 5 weeks, two groups were identified: 47 (group 1) who showed a significant (beyond the reproducibility limits) 7-month reduction of the resting perfusion defect, and 21 patients (group 2) in whom the perfusion defect remained unchanged. Ejection fraction and the extent of abnormal wall motion significantly (P < .01) improved in group 1 but not in group 2. Despite the presence of a comparable perfusion defect size between the two groups at 5 weeks after infarction, group 1 already showed a better regional and global ventricular function (P < .05). No significant differences were found between the two groups regarding age, medical therapy, the extent of underlying coronary disease, thrombolysis in the acute phase, Thrombolysis in Myocardial Infarction grade of the infarct-related vessel, and presence of collaterals on angiography. CONCLUSIONS: After anterior Q-wave infarction, the recovery of perfusion and wall motion may continue well after the subacute phase. Several patients exhibit relative hypoperfusion in viable tissue as late as 5 weeks after infarction, and a significant improvement of perfusion in the infarcted area commonly is observed between 5 weeks and 7 months. This delayed improvement of perfusion is associated with a delayed improvement of contractile function in the infarcted area after the first 5 weeks, which may continue for up to 7 months, suggesting the presence of hibernating myocardium in the infarcted area. Despite similar perfusion defect sizes, the level of regional function can be different at 5 weeks, and measurements taken around this time may not accurately estimate the eventual recovery of function.

Adult↗

PubMed1993

Long-term physical training and left ventricular remodeling after anterior myocardial infarction: results of the Exercise in Anterior Myocardial Infarction (EAMI) trial. EAMI Study Group.

OBJECTIVES: The aim of this multicenter randomized study was to investigate whether long-term physical training would influence left ventricular remodeling after anterior myocardial infarction. BACKGROUND: Exercise is currently recommended for patients after myocardial infarction; however, the effects of long-term physical training on ventricular size and remodeling still have to be defined. METHODS: Patients with no contraindications to exercise were studied 4 to 8 weeks after anterior Q wave myocardial infarction and 6 months later by echocardiography at rest and bicycle ergometric testing. After the initial study, patients were randomly allocated to a 6-month exercise training program (n = 49) or a control group (n = 46). A computerized system was used to derive echocardiographic variables of ventricular size, function and topography. RESULTS: After 6 months, a significant (p < 0.01) increase in work capacity (from 4,596 +/- 1,246 to 5,508 +/- 1,335 kp-m) was observed only in the training group, whereas global ventricular size, regional dilation and shape distortion did not change in either the control or the training group. However, compared with patients with an ejection fraction > 40%, patients with an ejection fraction < or = 40% had more significant (p < 0.001) ventricular enlargement at entry and demonstrated further (p < 0.01) global and regional dilation after 6 months, in both the control and the training group (end-diastolic volume from 77 +/- 14 to 85 +/- 17 ml/m2 in the control group and from 74 +/- 11 to 77 +/- 15 ml/m2 in the training group; regional dilation from 46 +/- 18% to 57 +/- 21% in the control group and from 42 +/- 18% to 44 +/- 26% in the training group). Ventricular size and topography did not change in patients with an ejection fraction > 40%. CONCLUSIONS: Patients with poor left ventricular function 1 to 2 months after anterior myocardial infarction are prone to further global and regional dilation. Exercise training does not appear to influence this spontaneous deterioration. Thus, postinfarction patients without clinical complications, even those with a large anterior infarction, may benefit from long-term physical training without any additional negative effect on ventricular size and topography.

Electrocardiography↗

PubMed1992

EAMI--exercise training in anterior myocardial infarction: an ongoing multicenter randomized study. Preliminary results on left ventricular function and remodeling. The EAMI Study Group.

To determine the effects of a 6-month exercise training program on left ventricular (LV) function and remodeling, 49 consecutive patients (pts) with first Q anterior myocardial infarction (51 +/- 8 years), in I-II NYHA class, were studied 4 to 8 weeks after the acute episode and 6 months later by 2D-ECHO and upright bicycle ergometric test. At entry, pts were randomly allocated to physical training (T = 25pts) or control (C = 24pts). Global endocardial surface area (ESA), LV volumes and EF, extent of abnormal wall motion (%WMA), of regional dilatation (%REG DIL), and the shape distortion (DIST) index were analyzed. After 6 months, a significant increase in work capacity (4,589 +/- 1,417 to 5,379 +/- 1,485 KPM/min, p less than 0.03) and in lactic anaerobic threshold (45 +/- 13 to 63 +/- 15 W, p less than 0.01) was observed only in T. Initial ESA, EDV, EF, %WMA, %REG DIL, and DIST index were similar and they did not change after 6 months in both groups. However, pts with less than 40%EF had greater (p less than 0.0001) EDV and %WMA with marked DIST index at entry and showed further (p less than 0.01) deterioration after 6 months both in C and in T (EDV, ml/m2: 68 +/- 12 to 77 +/- 18 in C, 71 +/- 12 to 74 +/- 18 in T; %REG DIL: 39 +/- 20 to 49 +/- 24 in C, 32 +/- 12 to 35 +/- 23 in T; DIST index: 0.16 +/- 0.07 to 0.21 +/- 0.09 in C, 0.2 +/- 0.07 to 0.22 +/- 0.1 in T). These variables did not change in pts with greater than 40%EF. Thus, from these preliminary data, pts with less than 40%EF at entry are prone to further global and regional LV deterioration. Physical training does not seem to increase this spontaneous deterioration.

Anaerobic Threshold↗

PubMed1991

Influence of mental stress on ventricular pump function in postinfarction patients. An invasive hemodynamic investigation.

To assess the influence of mental stress on ventricular pump function in coronary patients, 88 postinfarction patients (mean age, 53 +/- 10 years) performed mental arithmetic during Swan-Ganz catheterization monitoring a mean of 44 +/- 16 days after myocardial infarction. The test lasted 3 minutes in 66 patients and 10 minutes in 22 patients. Two patients suffered acute pulmonary edema a few minutes after mental arithmetic, but no others complained of symptoms. Mean heart rate increased from 76 +/- 14 to 92 +/- 17 beats/min, mean systolic blood pressure increased from 138 +/- 22 to 160 +/- 27 mm Hg, mean diastolic blood pressure increased from 89 +/- 10 to 101 +/- 15 mm Hg, mean pulmonary wedge pressure increased from 13 +/- 6 to 19 +/- 8 mm Hg (p less than 0.001), and mean stroke volume decreased from 72 +/- 18 to 65 +/- 18 ml (p less than 0.001) during mental arithmetic. The changes in central hemodynamics during mental arithmetic were not predictable from noninvasive parameters. In the 22 patients who performed 10-minute mental arithmetic, the changes persisted throughout mental exercise. Eighty-one patients underwent supine bicycle ergometry after mental arithmetic: Absolute mental arithmetic-pulmonary wedge pressure values correlated with those during exercise at the first stage (25 W) (r = 0.63, p less than 0.001) and at maximal load (77 +/- 29 W) (r = 0.49, p less than 0.001), and pulmonary wedge pressure change between stress values and baseline during mental arithmetic did not correlate with those during the first stage of exercise (r = 0.09, p = NS) or during maximal load (r = 0.11, p = NS). Twenty-nine patients repeated the study 1 year after myocardial infarction, and the same hemodynamic changes were observed during mental arithmetic. In conclusion, it appears that mental stress can cause deteriorations of central hemodynamics that can be independent of changes in heart rate and blood pressure and are not predictable from exercise-induced changes; stress-induced cardiovascular activation can last for at least 10 minutes and is stable over long time periods.

Adult↗

PubMed1991

Effects of mental exercise in patients with dilated cardiomyopathy and congestive heart failure. An echocardiographic Doppler study.

To assess the effects of mental stress on left ventricular diastolic function in patients with congestive heart failure, nine patients aged 57 +/- 12 years with dilated cardiomyopathy (end-diastolic volume, more than 110 ml/m2; ejection fraction, less than 40%; mean, 28 +/- 8%) and congestive heart failure in New York Heart Association functional class II or III and 14 normal volunteers (mean age, 49 +/- 8 years) were studied during mental arithmetic lasting 10 minutes with echocardiographic Doppler monitoring of transmitral flow velocity. During mental arithmetic, the ratio of peak flow velocity in early versus late diastole (E/A) and deceleration time of early diastole did not change in normal controls. However, E/A increased significantly (from 1.6 +/- 1.5 to 1.9 +/- 1.7; p less than 0.01) and deceleration time markedly decreased (from 156 +/- 49 to 108 +/- 31 msec; p less than 0.001) in patients with congestive heart failure. In 16 postinfarct patients with ejection fraction of less than 40% studied during mental arithmetic with simultaneous hemodynamics and Doppler recordings, good correlations were found between pulmonary wedge pressure and Doppler parameters (wedge pressure versus E/A, r = 0.89; wedge pressure versus deceleration time, r = -0.87). During mental arithmetic, the pulmonary wedge pressure-E/A correlation was weaker (r = 0.67), whereas the correlation between pulmonary wedge pressure and deceleration time was stronger (r = 0.91). The value of 153 msec in deceleration time was the best cutoff point in predicting 12 mm Hg pulmonary wedge pressure, both at rest and during mental arithmetic: the higher the deceleration time, the lower the pulmonary wedge pressure, and vice versa. Among patients with congestive heart failure, five showed normal baseline deceleration time (195 +/- 21 msec; pattern 1), and the remaining four showed a short (less than 153 msec) deceleration time (108 +/- 13 msec; pattern 2). During mental arithmetic, deceleration time markedly decreased to as short as 119 +/- 20 msec in all patients except one with baseline pattern 1. Deceleration time further decreased to 75 +/- 6 msec in all patients with baseline pattern 2. Mental arithmetic induces changes in left ventricular diastolic function in patients with congestive heart failure. Transmitral echocardiographic Doppler provides a simple noninvasive method of estimating and monitoring pulmonary wedge pressure in patients with severe left ventricular dysfunction.

Cardiomyopathy, Dilated↗

PubMed1989

Inaccuracy of various proposed electrocardiographic criteria in the diagnosis of apical myocardial infarction--a critical review.

The diagnostic accuracy of the standard electrocardiogram (ECG) in apical myocardial infarction (MI) was evaluated in 112 consecutive patients with recent MI and wall-motion abnormalities limited to the left ventricular (LV) apex on two-dimensional echocardiography, performed at rest 21 to 84 days after MI. The following patterns of abnormal (greater than or equal to 30 ms) Q waves were found: anteroseptal (Q V1-V4) in 44 patients (39.3%), anterolateral (Q V1-V6 and/or I, aVL) in 22 (19.6%), inferior (Q III, aVF or II, III, aVF) in five (4.5%), lateral (Q I, aVL and/or V5-V6) in five (4.5%), anteroinferior in six (5.3%); non-Q MI was present in 30 patients (26.8%). By applying various proposed ECG criteria, the presence of apical MI was correctly identified in very few (24, 21%) patients. LV apex was extensively asynergic in 85 patients (76%) and partially asynergic in 27 (24%). All the patients with Q waves in lateral leads and 47% of the patients with non-Q MI had partially asynergic LV apex, while in the other ECG patterns, extensively asynergic LV apex was predominant. The presence of both greater than or equal to 30 ms Q waves and loss of R in left precordial leads and I strongly suggests extensive apical asynergy; normal QRS in the same leads, however, does not exclude extensive apical involvement.(ABSTRACT TRUNCATED AT 250 WORDS)

Diagnostic Errors↗

PubMed1989

[Echocardiographic and electrocardiographic aspects indicative of necrosis caused by isolated disease of the right and circumflex coronary artery].

The value of 12-lead electrocardiogram (ECG) and two-dimensional echocardiography (2D-ECHO, wall motion abnormalities) in recognizing myocardial infarction due to left circumflex and right coronary artery disease was evaluated in 75 patients (aged 26-69 years, within 3 months of myocardial infarction) with single vessel disease (luminal stenosis greater than or equal to 70%). Twenty-five patients (pts) had left circumflex disease and 50 right coronary artery disease. In the group of pts with left circumflex disease, 13 (52%)--group I--showed asynergy limited to the postero-lateral wall and 12 pts (48%)--group II--had more extensive asynergy involving both the postero-lateral and the infero-posterior wall. No pts with left circumflex disease demonstrated asynergy of the interventricular septum. Good correlations were found between the site and extent of asynergy and the location of left circumflex narrowings: 9--group I pts--(69.2%) had obtuse marginal branch disease and 8--group II pts--(67%) had proximal left circumflex disease. Patients with right coronary artery disease were subdivided as follows: group I: 35 pts (70%) with asynergy of infero-posterior wall and posterior septum; group II: 11 pts (22%) with extensive asynergy of infero-posterior, postero-lateral walls and posterior septum; group III: 4 pts (8%) with asynergy limited to the infero-posterior wall. The location of right coronary artery narrowings had no relation to the site and extent of infarct asynergy in pts with single right coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗