Segmental Wall Motion Score Research Articles

Dobutamine stress echocardiography at 7.5 μg/kg/min using color tissue Doppler imaging M-mode safely predicts reversible dysfunction early after reperfusion in patients with acute myocardial infarction

Dobutamine stress echocardiography (DSE) is widely used to predict reversible left ventricular dysfunction, but evaluation by this method is subjective. The recently developed color tissue Doppler imaging (TDI) M-mode may permit objective and quantitative assessment of changes in wall motion induced by DSE. We tested the hypothesis that this new method can detect sensitively reversible dysfunction in the post–myocardial infarction setting. DSE with color TDI M-mode and conventional DSE were performed to predict reversible dysfunction in 53 patients at a mean of 3 days after infarction using 7.5 and 10 μg/kg/min of dobutamine. Follow-up regular echocardiography (4 weeks later) was used as the reference technique to define reversible dysfunction segments. To predict reversible dysfunction segments, the standard segmental wall motion score change on conventional DSE and the ratio of the segmental wall velocity difference at rest versus stress (7.5 and 10 μg/kg/min) on DSE with color TDI M-mode (7.5-TDI-M and 10-TDI-M, respectively) were used. With 7.5 μg/kg/min of dobutamine, the sensitivity for predicting reversible dysfunction using color TDI M-mode (7.5-TDI-M) was significantly higher than that of conventional DSE (89% vs 73%, p <0.05) whereas specificities and predictive values were almost identical. With a 10-μg/kg/min dose, color TDI-M mode (10-TDI-M) and conventional DSE were not significantly different in predicting reversible dysfunction. With use of color TDI-M mode, regional wall motion during DSE was analyzed objectively and quantitatively. Moreover, combined TDI-M and conventional data were slightly superior to either mode alone. There were no arrhythmias during 7.5 μg/kg/min of dobutamine, but 9 arrhythmias occurred during the 10-μg/kg/min dose in patients with acute myocardial infarction. In conclusion, color TDI M-mode permits objective and quantitative assessment of regional ventricular wall motion and gives additional information for detecting reversible dysfunction in DSE. Improvement of sensitivity at a lower dose of dobutamine with color TDI-M mode may increase the safety of DSE in the post–myocardial infarction setting.

Combined assessment of myocardial perfusion and left ventricular function with exercise technetium-99m sestamibi gated single-photon emission computed tomography can differentiate between ischemic and nonischemic dilated cardiomyopathy

The purpose of this study was to determine whether exercise technetium-99m sestamibi gated single-photon emission computed tomography (SPECT) accurately distinguishes between patients with ischemic cardiomyopathy and patients with nonischemic left ventricular systolic dysfunction. Noninvasive tests have previously failed to accurately separate patients with ischemic cardiomyopathy from those with nonischemic cardiomyopathy. Technetium-99m gated SPECT imaging offers advantages that have the potential to overcome the limitations of previous studies. Thirty-seven adults with a left ventricular ejection fraction ≤ 35%, including 24 patients with nonischemic cardiomyopathy and 13 patients with ischemic cardiomyopathy, were prospectively evaluated using symptom-limited metabolic exercise treadmill testing with technetium-99m sestamibi gated SPECT imaging. Interpretation of myocardial perfusion and regional wall motion was performed, using a 17-segment model. Summed stress, rest, and reversibility perfusion defect scores were determined, and the variance of segmental wall motion scores was computed. Summed stress, rest, and reversibility perfusion defect scores were significantly lower in nonischemic cardiomyopathy patients, compared with those with ischemic cardiomyopathy (summed stress defect score: 6.9 ± 3.8 vs 32.9 ± 7.7, respectively, p < 0.001). Variability in segmental wall motion was also significantly lower in patients with nonischemic cardiomyopathy compared with those with ischemic cardiomyopathy (variance: 0.3 ± 0.3 vs 1.2 ± 0.8, respectively, p < 0.001). Thus, assessment of myocardial perfusion and regional ventricular function with exercise technetium-99m sestamibi gated SPECT imaging can reliably distinguish between patients with ischemic cardiomyopathy and patients with non-ischemic dilated cardiomyopathy.

Transmyocardial laser revascularisation in acutely ischaemic myocardium.

Although recent experience suggests that transmyocardial laser revascularisation (TMLR) relieves angina, its mechanism of action remains undefined. We examined its functional effects and analysed its morphological features in an animal model of acute ischaemia. A total of 15 pigs were randomised to ligation of left marginal arteries (infarction group, n = 5), to TMLR of the left lateral wall using a holmium:yttrium-aluminium garnet (Ho:YAG) laser (laser group, n = 5), and to both (laser-infarction group, n = 5). All the animals were sacrificed 1 month after the procedure. Haemodynamics and echocardiography with segmental wall motion score were carried out at both time intervals (scale 0-3: 0, normal; 1, hypokinesia; 2, akinesia; 3, dyskinesia). Histology of the involved area was analysed. Laser group showed no change of the segmental wall motion score of the involved area 30 min after the laser channels were made (score: 0 +/- 0). Infarction and laser infarction groups both showed a persistent and definitive increase of the segmental wall motion score (at 30 min: 1.6 +/- 0.3 and 2 +/- 0, respectively; at 1 month: 1.8 +/- 0.2 and 1.8 +/- 0.4, respectively). These increases were all statistically significant in comparison with baseline values (P < 0.5), however comparison between infarction and laser-infarction groups showed no significant difference. On macroscopic examination of the endocardial surface, no channel was opened. On histology, there were signs of neovascularisation around the channels in the laser group, whereas in the laser-infarction group the channels were embedded in the infarction scar. In this acute pig model, TMLR did not provide improvement of contractility of the ischaemic myocardium. To the degree that the present study pertains to the clinical setting, the results suggest that mechanisms other than blood flow through the channels should be considered, such as a laser-induced triggering of neovascularisation or neural destruction.

Left ventricular aneurysm repair: an assessment of surgical treatment modalities.

Different closure techniques (linear vs. circular), as well as the efficacy of revascularization in the left ventricular aneurysm repair, with regard to immediate and mid-term results, were assessed and factors having influence on the early mortality and morbidity and survival were analyzed. Between January 1991 and November 1996, 248 patients underwent surgical repair for postischemic left ventricular aneurysm. A total of 26 of them were female (10.50%). Linear closure was employed in 121 patients (48.8 %) and circular (patch endoaneurysmorraphy) closure in 127 (51.2%). Coronary revascularization was added in 203 (81.9%) cases. Patients were followed for an average follow-up time of 39.3 months. Early mortality rate was 6% (15 patients). The difference in mortality rate by the repair method was not statistically significant (8.3% in the linear closure group and 3.9% in the circular closure group, P = 0.15). Absence of preoperative angina pectoris (P = 0.029), dyspnea as the presenting symptom, a preoperative left ventricular segmental wall motion scoring of 14 or greater, a cardiopulmonary bypass duration exceeding 2 h (P = 0.004), an aortic clamping time exceeding 1 h (P = 0.026) were associated with early mortality. Concomitant coronary revascularization had no effect on early mortality. However, low cardiac output state was less frequent in patients with concomitant coronary revascularization (P = 0.022). Functional status improved in both groups. Follow-up extending to 81st month revealed no difference in survival between the groups (84% for linear closure group and 92% in circular closure group, including operative mortality, P = 0.12). However, functional status improvement was better in the patients who underwent circular repair (P = 0.0077). Revascularization appeared as having no important influence on both survival and functional status. A preoperative left ventricular segmental wall motion scoring of 14 or greater was associated with a higher incidence of early mortality, low cardiac output syndrome and poor long-term survival. Left ventricular aneurysm repair is an important therapeutic intervention and can be performed with reliable results, regardless of repair method, either linear or circular. Long term results revealed better functional status in circular repair group. Concomitant coronary revascularization reduced the incidence of low cardiac output state. Performance of the unaffected regions of myocardium was found to be an important determinant of both early and late outcome.

F18-fluorodeoxyglucose single-photon emission computed tomography predicts functional outcome of dyssynergic myocardium after surgical revascularization

Background. Prediction of functional recovery after revascularization is possible with positron emission tomography and F18-fluorodeoxyglucose (FDG). Recently, the use of FDG in combination with single-photon emission computed tomography (SPECT), with 511 keV collimators, has been proposed to allow more widespread use of FDG. In the current study we aimed to predict improvement of regional left ventricular function after surgical revascularization with FDG and SPECT. Methods and Results. Twenty-seven patients with regional wall motion abnormalities (on echocardiography) underwent early thallium-201 (T1-201) SPECT to assess perfusion and FDG SPECT to assess regional glucose uptake. The left ventricular myocardium was divided into 13 segments. For each segment, tracer uptake was evaluated visually (with the use of a 4-point scoring system) by consensus of two observers. Myocardial viability was determined in dyssynergic segments on echocardiography and defined as normal perfusion or increased FDG uptake in a perfusion defect (mismatch). Absence of viability was defined as a perfusion defect without increased FDG uptake (match). Improvement of regional wall motion was assessed 3 months after revascularization. In the group of segments that were viable on FDG/T1-201 SPECT ( n = 64), the segmental wall motion score decreased from 1.4 ± 0.5 to 0.6 ± 0.7 ( p < 0.01), whereas the segmental wall motion score remained unchanged in nonviable segments ( n = 72): 1.6 ± 0.5 versus 1.5 ± 0.6 (not significant). Forty-six (72%) of the 64 segments that were viable on FDG/T1-201 SPECT demonstrated improved contractile function after coronary revascularization. In contrast, only 7 (10%) of 72 nonviable segments on FDG/T1-201 SPECT showed improvement in function after revascularization ( p < 0.01 versus viable segments). The sensitivity, specificity, and positive and negative predictive values were 87%, 78%, 72%, and 90%, respectively. Conclusion. This study shows that FDG/T1-201 SPECT can identify patients who improve in regional ventricular function after revascularization.

Exogenous insulin-like growth factor II enhances post-infarction regional myocardial function in swine

Insulin-like growth factor II (IGF-II) promotes cardiac myocyte growth and contractility in vitro. This study was designed to investigate the effect of exogenous IGF-II on regional myocardial function at the area of infarct in the pig. Myocardial infarction was induced in 12 female anaesthetized pigs by affigel blue beads, embolizing microvessels of the left anterior descending coronary artery distribution. In the experimental group (n = 6), IGF-II (0.12 microgram.kg-1 in two animals and 0.6 microgram.kg-1 in four) was incorporated into the beads and delivered by them to the infarct area. Myocardial function was followed echocardiographically, and the excised heart was analysed immunohistochemically and histopathologically. Myocardial function in injured zones, inversely related to an echocardiographic segmental wall motion score (mean +/- SEM), was similar between the two groups at baseline, but at 4 weeks post-infarction was significantly (P = 0.008) reduced in the control group (0.58 +/- 0.38 vs 3.42 +/- 0.84), in contrast to nearly baseline values in the experimental group (0.58 +/- 0.33 vs 1.17 +/- 0.42, P = 0.41). Cardiac performance in injured segments was significantly better after myocardial injury in the experimental group (P = 0.04). Tissue samples from both groups (4 weeks post-infarction), stained with haematoxylin and eosin demonstrated peri-infarct myocyte hypertrophy, corresponding to regions selectively stained by an antibody for CD56, which highlights growing cardiac myocytes. By image analysis semi-quantification, staining for CD56 was significantly (P = 0.04) higher in the peri-infarct region of the experimental group, as compared with controls (106.5 +/- 2.8 vs 92 +/- 4.4 gray level units). Microvessels stained for von-Willebrand factor were similar in number in both groups (P = 0.8), as were mesenchymal cells stained for vimentin (P = 0.7). Exogenous IGF-II, delivered to the infarct area ameliorates regional cardiac function in the pig, perhaps by inducing peri-infarct myocyte growth.

811-2 Evidence that Myocardial Stunning Occurs in Humans Following Unstable Angina

Reversible postischemic dysfunction, or myocardial stunning, is a well defined experimental entity which is characterized by the presence of a perfusion-contraction mismatch, i.e. the persistence of segmental dysfunction despite complete restoration of nutritive perfusion. Reversible dysfunction occurs following ischemic syndromes such as non-Q wave infarction, unstable angina, cardio-pulmonary bypass. Definite demonstration that reversible dysfunction indeed represents myocardial stunning is lacking, owing to the difficulty of measuring myocardial blood flow (MBF) in absolute terms. Therefore, we measured regional wall motion (by 2D echo) and absolute MBF with 13 N-ammonia and positron emission tomography (PET) in 11 patients with unstable angina, Despite successful PTCA of the culprit lesion on the left anterior descending coronary artery, all patients showed persistent anterior. wall dysfunction at the time of the PET study (within 48 hours after PTCA). As judged from the changes in segmental wall motion (in 6 ± 2 abnormal segments, mean ± sd, out of 16 in each patient) from the time of PET study to 4–8 weeks later, regional dysfunction was entirely reversible in 9/11 patients. In these 9 patients, the segmental wall motion score improved from 2.4 ± 0.3 to 1.2 ± 0.1 at late follow-up. With PET, 13 N-ammonia MBF was within the normal range in 8/9 patients (95 ± 21 ml/min/l00 g, range 60124 ml/min/l 00 g), while it was decreased (33 ml/min/l00 g) in the remaining patient. On average, in the 9 patients, absolute MBF was similar among stunned and remote normally contracting myocardial segments (88 ± 28 vs 85 ± 25 ml/min/100 g, p = ns). Our data thus show perfusion-contraction mismatch, confirming that myocardial stunning can occur in humans following attacks of unstable angina.

Collateral circulation in total occlusion of the left anterior descending or right coronary artery.

The functional significance of the collateral circulation was evaluated in 125 patients with total coronary occlusion. Patients were classified into two groups. Group 1:patients with angina pectoris (AP), Group 2:patients with a first transmural myocardial infarction (MI) within 3 months of the symptom onset. Clinical variables, resting and exercise electrocardiogram (EKG) were analyzed with angiographic findings. Collateral fillings were graded from 0 to 3: 0 = none; 1 = filling of side branches only; 2 = partial filling of the epicardial segment; 3 = complete filling of epicardial segment. The wall motion of each segment was scored from 1 to 5: 1 = normal; 2 = mild to moderate hypokinesia; 3 = severe hypokinesia; 4 = akinesia; 5 = dyskinesia. The scores of the 5 segments were added to yield a total LV score. There was a higher prevalence of good collaterals and multi-vessel disease in patients with AP than in those with MI (83% vs 53%, 54% vs 30%, respectively, p < 0.005). The left ventricular ejection fraction (LVEF), left ventricular end-diastolic pressure (LVEDP) and segmental wall motion score were significantly better in patients with AP than in those with MI (68.9 +/- 13.4%, vs 50.5 +/- 12.6%, 15.0 +/- 7.3 mmHg vs 20.3 +/- 8.8 mmHg, 6.5 +/- 2.2 vs 9.6 +/- 2.3, respectively, p < 0.05). In spite of total coronary occlusion, 61% of AP patients had normal resting EKG but (96% of AP patients who underwent treadmill test proved positive. The proportions of well-developed collaterals in 3 groups divided according to the interval between onset of MI and angiography (within 1 day, 2 to 14 days, 15 days to 3 months) were 13%, 54% and 60%. There were no significant differences in LVEF, segmental wall motion score and LVEDP in MI patients with poorly-developed collaterals and well-developed collaterals (49.1 +/- 15.7% vs 46.4 +/- 10.1%, 11.1 +/- 2.2 vs 10.9 +/- 1.4 and 24.3 +/- 9.7 mmHg vs 20.3 +/- 7.0 mmHg, p = NS). The degree of collateral development was higher in MI with right coronary artery occlusion compared with that of left anterior descending artery occlusion (1.1 +/- 1.0 vs 2.0 +/- 1.0, p < 0.05). In conclusion, collateral circulation can prevent myocardial ischemia and preserve myocardial function in a significant number of patients with AP but do not provide protection against exercise-induced myocardial ischemia in the majority of patients with AP.(ABSTRACT TRUNCATED AT 400 WORDS)

Functional Significance of Collateral Circulation in Patients with Total Coronary Occlusion

Functional significance of collateral circulation was evaluated in 125 patients with total coronary occlusion. Patients were classified into 2 groups: group 1, patients without myocardial infarction; and group 2, patients with a first transmural myocardial infarction occurring within 3 months of symptom onset. There was a higher prevalence of well-developed collaterals and multivessel disease in patients without myocardial infarction than in those with myocardial infarction. The left ventricular ejection fraction, left ventricular enddiastolic pressure, and segmental wall motion scores were significantly better in group 1 than group 2. Despite total coronary occlusion, 61% of group 1 had a normal resting electrocardiogram; however, 96% of patients who underwent treadmill tests proved positive. The proportions of well-developed collaterals in 3 groups, divided according to the internal between onset of myocardial infarction and angiography (within 1 day of operation, 2 to 14 days, or 15 days to 3 months), were 13%, 54%, and 60%. There were no significant differences in left ventricular ejection fraction, segmental wall motion score, and left ventricular enddiastolic pressure in myocardial infarction patients with poorly developed collaterals and well-developed collaterals. The degree of collateral development is higher in myocardial infarction with right coronary artery occlusion compared with that of left anterior descending artery occlusion, without regarding the dominancy or length. Collateral circulation can prevent myocardial ischemia and present myocardial function in a significant number of patients without infarction; however, it does not provide protection against exercise-induced myocardial ischemia in the majority of patients from group 1. Although well-developed collaterals are not usually present within 1 day after myocardial infarction, they are generally present after 2 weeks. Collateral vessels in patients with myocardial infarction have no beneficial effects on preserving myocardial function.

Utility and limitations of linear models for echocardiographic estimation of left ventricular ejection fraction by segmental wall-motion scoring. A geometric analysis.

Although the geometric relation between left ventricular (LV) volume and its internal dimensions is nonlinear, recent clinical study has shown that LV ejection fraction (EF) predicted by a linear combination of segmental contraction scores correlates well with the EF by radionuclide angiography. To determine whether the linear coefficients found by empirical study are consistent with basic geometric principles, we compared the LV EF obtained by exact geometric calculation to the EF predicted using a simple linear combination of segmental contraction scores over a wide range of segmental function, from marked dyskinesis to marked hyperkinesis. We found that an optimal linear equation for global EF on geometric grounds is: Global EF = 4 + 0.28xC1 + 0.24xC2 + 0.12xC3, where C1, C2, and C3 are the mean segmental contraction scores at the base, mid-left ventricle, and the apex, respectively. The EF predicted by this formula differs by less than 6 percentage points from the EF predicted by exact geometry when segmental contraction ranges from normal to akinetic, and the coefficients are in close accord with those found empirically by regression of linearly-derived EFs against the radionuclide EFs in 50 patients. However, when segmental contraction is significantly hyperkinetic or dyskinetic, agreement with the exact geometric formula is poor. We conclude that: (1) a linear combination of segmental contraction scores can provide reasonable estimates of LV EF over a broad range of contraction; (2) previous, empirically determined linear coefficients are consistent with geometric principles; and (3) exact, nonlinear formulas may be required for ventricles with significant degrees of hyperkinesis or dyskinesis.

Comparison with radionuclide angiography of two new geometric and four nongeometric models for echocardiographic estimation of left ventricular ejection fraction using segmental wall motion scoring

Two new eehocardlographic methods for estimating left ventricular ejection fraction, both based on segmental wall motion scoring on a continuous scale, were developed and compared to radionu-clide angiography in 50 patients. The first method used a geometric model in which the ventricle was represented by a tubular base section joined to a hemielliptical apex section, each containing 4 quadrants. Contraction was scored visually in 12 regions of the ventricle. The 12 scores were converted to dimensional shortenings, which were then used to calculate separate ejection fractions for each of the 8 quadrants. These 8 values were averaged to obtain the global ejection fraction. AssumIng an elliptical end-systolic cross-section shape for each quadrant, the correlation between the echocardiographic and radionuclide ejection fractions was 0.917 with a regression slope of 0.93 and an intercept of 1.5. Results were identical assuming circular end-systolic quadrant shapes. The second approach used a linear combination of the mean wall motion score at the base, midleft ventricle and apex to predict ejection fraction. Coefficients for the 3 mean scores were optimized by least squares least fit with radionuclide ejection fraction In all 50 patients. The simplest Linear model showed a correlation of 0.90 between the echocardiographic and radionuclide ejection fraction but underestimated low, and overestimated high, ejection fractions. However, these systematic errors could be removed by regression, which added a constant term of 8.1 and a slope factor of 0.87 to the linear model, improving the correlation with radionuclide ejection fraction to 0.91. Segmental wall motion scoring on a continuous scale with an appropriate geometric model can provide good estimates of ejection fraction if each ventricular quadrant is analyzed separately and the results are averaged. Properly weighted linear combinations of the contraction scores provide comparably accurate estimates of the ejection fraction.

Long-Term Clinical, Hemodynamic, Angiographic, and Neurohumoral Responses to Vasodilation with Felodipine in Patients with Chronic Congestive Heart Failure

Twenty patients on conventional therapy for severe congestive heart failure (CHF) were randomly assigned to adjunctive treatment with felodipine (n = 10) or placebo (n = 10) and followed over a 6-month period. Baseline clinical, hemodynamic, angiographic, and neurohumoral estimates of CHF were comparable in the two treatment groups. These estimates remained virtually unchanged at 6 months in patients on placebo therapy, but circulating noradrenaline levels were further augmented. In patients on felodipine therapy, substantial reductions in left ventricular end-systolic pressure, mean arterial pressure, and systemic vascular resistance were observed at 6 months. This afterload reduction led to a preferential increment in the stroke volume (36%) which increased cardiac output (30%), whereas heart rate tended to decrease. The improved hemodynamics during felodipine treatment were paralleled by marked improvements in the angiographic left ventricular ejection fraction and regional segmental wall motion score. The enhanced contractile state of the left ventricle was accompanied by significant reductions in the augmented plasma levels of catecholamines, and the patient clinical status improved. The 6-month mortality rate in the 20 patients was 40% and indicated a closer relation to baseline noradrenaline plasma levels than to hemodynamic or angiographic estimates of CHF. Despite the limited number of patients, the long-term clinical efficacy of felodipine is thus evidenced in patients with CHF and is related to sustained arteriolar dilatation and improved neurohumoral profile by this vasoselective calcium antagonist.

Left ventricular segmental wall motion score as a criterion for selecting patients for direct surgery in the treatment of postinfarction ventricular tachycardia.

No indisputable criteria for selecting candidates for direct surgery in postinfarction ventricular tachycardia are yet available. We prospectively tested the result of surgery in patients showing normokinesia or slight hypokinesia in at least 3 of 9 segments of the left ventricle as determined on two oblique projections of the left ventricular angiogram. Sixty consecutive patients with recurrent symptomatic ventricular tachycardia were stratified on the basis of this criterion; 50 candidates were thus eligible for surgery. Direct surgery (endocardial resection and/or cryoablation) was performed in 23 patients (after a mean of 4.1 antiarrhythmic drug trials), while 27 patients were maintained on drug treatment (at discharge, a mean of 3.7 drug trials). Surgery was map-guided in 19 patients and non-map-guided in four emergency cases. No patients died in the immediate postoperative phase, but two (9%) died during follow-up. The actuarial survival at 12 months was 93%; the surgery-alone cure rate for ventricular tachycardia was 78%. Of the 27 non-operated surgical candidates, two died during in-hospital drug testing and five after discharge (total 26%). Actuarial survival at 12 months was 78% and did not differ significantly from that of the operated patients. After discharge, 80% of the non-operated surgical candidates still using the drug at discharge remained free of recurrence. In the 10 drug-treated non-surgical candidates (at discharge, a mean of 3.8 drug trials), survival and the number of arrhythmia-free patients were markedly lower than in surgical candidates. This study shows that the segmental wall motion score is of great clinical value and can be applied for stratification of patients with ventricular tachycardia after myocardial infarction for either surgery or medical therapy.

Surgical Survival in the Coronary Artery Surgery Study (CASS) Registry

The overall surgical survival data in the Coronary Artery Surgery Study (CASS) registry have not been published to date, pending the report of the randomized medical-surgical comparison (CASS randomized trial). Non-randomized surgical survival data from the CASS registry are given in this article. The overall medical survival data from the registry were reported previously as a natural history study. There were 8,991 patients in the registry portion of CASS who had primary isolated coronary artery bypass grafting and 8,971 with follow-up of more than 30 days. The 5-year survival for all 8,971 patients was 90%, and the operative mortality was 2.37%. Patients with left main coronary artery disease had an operative mortality of 3.84% and a 5-year survival of 85%, while patients with lesions in other vessels had an operative mortality of 2.12% and a 5-year survival of 91%. Among patients without left main coronary disease, the 5-year survival was 93% in those with single-vessel and 92% in those with double-vessel disease (operative mortality was 1.50% and 1.92%, respectively) and 88% in patients with triple-vessel disease (operative mortality was 2.62%; p = 0.009). When results for patients with left main coronary artery obstruction were compared with those for triple-vessel disease, the 5-year survival figures were 85% and 88%, respectively ( p = 0.02) and the operative mortality, 3.84% and 2.62%, respectively ( p = 0.03). Patients with normal or nearly normal left ventricular (LV) function (i.e., LV segmental wall motion scores ranging from 5 through 11) had a 5-year survival of 92% and an operative mortality of 1.97%. Patients with moderate impairment (LV score range, 12 through 16) had a 5-year survival of 80% and an operative mortality of 4.21%. In those with poor ventricular function (LV score of 17 or greater), the 5-year survival was 65% and the operative mortality was 6.21%. The difference in survival among the three groups was significant ( p < 0.0001). Of 29 variables used in a stepwise Cox regression analysis, LV wall motion score, congestive heart failure score, age, number of operable vessels, smoking history, LV end-diastolic pressure, and percent of left main coronary artery stenosis were found to have a significant effect on long-term survival (excluding 30-day mortality), and these variables plus surgical priority and height influenced surgical mortality. When height was used in the Cox proportional hazards model, female sex was no longer a significant variable.

Value of two-dimensional echocardiography in evaluating coronary artery disease: A randomized blinded analysis

Two-dimensional echocardiography at rest was used to analyze segmental wall motion abnormalities for detecting coronary artery disease in patients with and without a history of myocardial infarction. One hundred twenty-five echocardiograms were analyzed in a randomized, blinded fashion. They were obtained from 55 consecutive patients found to have significant coronary artery disease at angiography, 59 consecutive normal subjects and 11 patients with dilated cardiomyopathy. The overall sensitivity of two-dimensional echocardiography was relatively low at 67%. However, specificity was 99%. The sensitivity was higher in patients with past myocardial infarction than in those without myocardial infarction (81 versus 42%), as expected. Echocardiography can detect segmental wall motion abnormalities in some patients with coronary artery disease and no overt prior myocardial infarction. This was highlighted by nine such patients with coronary artery disease and no prior myocardial infarction or electrocardiographic Q waves who were found to have segmental wall motion abnormalities. A semiquantitative, two-dimensional echocardiographic segmental wall motion score was derived for 47 patients and was correlated with angiographic left ventricular ejection fraction (r = 0.71). This score differentiated patients with a normal ejection fraction (greater than 50%) from those with a depressed ejection fraction (less than 50%): 1.1 +/- 1.6 versus 6.9 +/- 3.1 (p less than 0.001). Almost all patients (92%) with an echocardiographic score of five or more had an abnormal ejection fraction of less than 50%. In patients with chronic congestive heart failure, the echocardiogram separated those with dilated cardiomyopathy from those with coronary artery disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Two-dimensional echocardiographic analysis of segmental left ventricular wall motion before and after coronary artery bypass surgery.

Twenty patients with coronary artery disease were studied with two-dimensional echocardiography the day before saphenous vein bypass graft surgery. Serial studies were obtained 7.4 +/- 2.5 (+/- SD) and 43.4 +/- 13.1 days postoperatively to qualitatively assess the effect of bypass surgery on regional wall motion. Changes in segmental wall motion were assessed semiquantitatively by assigning a segmental wall motion score to each of nine echocardiographically defined segments. Preoperatively, 18% of the segments moved abnormally. The mean overall segmental wall motion score did not change significantly, as shown by comparing the postoperative studies with the preoperative study. However, there was a significant worsening in the septal motion (apical and basal) and a significant improvement in posterior wall motion (apical and basal) after bypass surgery. Anterior and lateral wall motion were not significantly changed. Nonseptal segments that were normal preoperatively usually remained normal; abnormal nonseptal segments usually improved or were unchanged by surgery. The motion of septal segments, however, generally worsened postoperatively whether they were normal or abnormal preoperatively. We conclude that segmental wall motion assessed by two-dimensional echocardiography may improve after revascularization surgery, but the interventricular septum shows impaired motion. This effect of coronary artery bypass on wall motion is better demonstrated relatively late after operation than early in the postoperative course, as has been done in some previous studies.

Effect of nifedipine on exercise-induced left ventricular dysfunction and myocardial hypoperfusion in stable angina

To assess the effects of nifedipine on left ventricular function and regional myocardial perfusion, exercise radionuclide ventriculography was performed in 15 men (median age 59 years) and exercise thallium-201 scintigraphy was done in 11 of them, before and 90 minutes after the oral administration of 20 mg of nifedipine. All patients had stable angina and angiographically proved coronary artery disease without evidence of spasm. Exercise tolerance after administration of nifedipine increased from 343 ± 42 seconds to 471 ± 50 seconds (p < 0.01), whereas the peak exercise double product remained essentially unchanged (difference not significant). Ejection fraction improved significantly at rest (from 49 ± 3.6% to 52 ± 3.3%, p < 0.05) and at peak exercise (42 ± 3.3% to 47 ± 3.7%, p < 0.05). Nifedipine also resulted in an improved segmental wall motion score (4.3 ± 2.3 to 3.0 ± 2.3, p < 0.05; 0 = normal and 4 = worst degree of dysfunction). The ejection fraction increased by more than 5% in one third of the patients at rest, and in more than half of the patients at peak exercise. Improved exercise myocardial perfusion occurred in 5 of 11 patients (45%) and in 7 of 28 segments (25%) with reversible hypoperfusion. Thus, nifedipine produces significant improvement in global and regional left ventricular function in patients with coronary artery disease and stable angina. This may be accounted for, at least in part, by improvement in myocardial perfusion.