Residual Myocardial Ischemia Research Articles

Prognostic interaction between viability and residual myocardial ischemia by dobutamine stress echocardiography in patients with acute myocardial infarction and mildly impaired left ventricular function

Dobutamine stress echocardiography (DSE) accurately detects viable myocardium and residual ischemia in patients with acute myocardial infarction (AMI). The prognostic interaction of viability and ischemia has not been completely clarified in these patients. This study assesses the long-term effect of viability, ischemia, or their combination on survival in patients with AMI and mildly impaired left ventricular (LV) function. Four hundred eleven patients (age 57 ± 9 years) underwent predischarge DSE (up to 40 μg/kg/min plus atropine if needed) after uncomplicated AMI and were prospectively followed for 23 months (range 1 to 78). According to DSE findings, patients were divided into 4 groups: viability only, ischemia only, combination of viability and ischemia, and scar. Adverse outcome occurred in 64 patients: 34 patients had hard events (9 cardiac deaths, 25 nonfatal AMI) and 30 patients had unstable angina requiring hospitalization. The combination of viability and ischemia, diabetes mellitus, and non–Q-wave AMI were significant predictors of all events at univariate and multivariate analysis. The same variables were also univariate predictors of hard events, but multivariate analysis indicated only the combination of viability and ischemia and diabetes as independent predictors. The event-free survival of patients with combined viability and ischemia was significantly lower (hazard ratio 3 [95% confidence interval 1.8 to 11]) compared with patients with ischemia only. Thus, viability and ischemia show a significant adverse prognostic interaction in patients with AMI and preserved LV function.

Thyroid and lipid metabolism.

Thyroid hormones influence all major metabolic pathways. Their most obvious and well-known action is an increase in basal energy expenditure obtained acting on protein, carbohydrate and lipid metabolism. With specific regard to lipid metabolism, thyroid hormones affect synthesis, mobilization and degradation of lipids, although degradation is influenced more than synthesis. The main and best-known effects on lipid metabolism include: (a) enhanced utilization of lipid substrates; (b) increase in the synthesis and mobilization of triglycerides stored in adipose tissue; (c) increase in the concentration of non-esterified fatty acids (NEFA); and (d) increase of lipoprotein-lipase activity. While severe hypothyroidism is usually associated with an increased serum concentration of total cholesterol and atherogenic lipoproteins, the occurrence of acute myocardial infarction (AMI) in hypothyroid patients is not frequent. However, hypothyroid patients appear to have an increased incidence of residual myocardial ischemia following AMI. Even in subclinical hypothyroidism, which is characterized by raised serum TSH levels with normal serum thyroid hormone concentrations, mild hyperlipidemia is present and may contribute to an increased risk of atherogenesis. Prudent substitution therapy with L-thyroxine is indicated in patients with both overt and subclinical hypothyroidism, with or without angina, to counteract the cardiovascular risk resulting from hyper-dyslipidemia.

Risk stratification after acute myocardial infarction in the reperfusion era

Historically, risk stratification for survivors of acute myocardial infarction (AMI) has centered on 3 principles: assessment of left ventricular function, detection of residual myocardial ischemia, and estimation of the risk for sudden cardiac death. Although these factors still have important prognostic implications for these patients, our ability to predict adverse cardiac events has significantly improved over the last several years. Recent studies have identified powerful predictors of adverse cardiac events available from the patient history, physical examination, initial electrocardiogram, and blood testing early in the evaluation of patients with AMI. Numerous studies performed in patients receiving early reperfusion therapy with either thrombolysis or primary angioplasty have emphasized the importance of a patent infarct related artery for long-term survival. The predictive value of a variety of noninvasive and invasive tests to predict myocardial electrical instability have been under active investigation in patients receiving early reperfusion therapy. The current understanding of the clinically important predictors of clinical outcomes in survivors of AMI is reviewed in this article. Copyright © 2000 by W.B. Saunders CompanyProgress in Cardiovascular Diseases, Vol. 42, No. 4 (January/February), 2000: pp 273-309

Basic principles of angiogenesis for the interventional cardiologist.

Despite tremendous advances in the management of coronary artery disease, there is a growing population of patients who remain symptomatic with residual myocardial ischemia. Therapeutic angiogenesis, designed to promote the development of endogenous conduits forming collateral blood vessels that serve to bypass coronary artery stenotic lesions, may constitute an alternative treatment strategy for patients with extensive tissue ischemia in whom contemporary therapies-antianginal medications, angioplasty, bypass surgery-have failed or are not feasible. Intensive investigation is now focused on methods that would have the potential to stimulate the development of collaterals in humans. In this review we summarize the physiology of angiogenesis and its role in development and adult life, its regulation, the effects of ischemia and hypoxia, the principles of gene therapy for angiogenesis, and an update on the current available trials data of angiogenic cytokines administration.

Significance of dobutamine-induced ST-segment elevation and T-wave pseudonormalization in patients with Q-wave myocardial infarction: simultaneous evaluation by dobutamine stress echocardiography and thallium-201 SPECT

The clinical significance of stress-induced ST-segment elevation and T-wave pseudonormalization in infarct-related leads is still controversial. Therefore, we conducted the present study to assess this issue using simultaneous dobutamine stress echocardiography (DSE) and thallium-201 single-photon emission computed tomography. A total of 119 patients with Q-wave myocardial infarction were enrolled in this study. There were 58 patients with (group I) and 61 patients without (group II) dobutamine-induced ST-T changes. Left ventricular ejection fraction was 43 ± 13% in group I and 49 ± 14% in group II (p <0.05). The baseline, low-, and peak-dose global wall motion scores were similar between these 2 groups (26.2 ± 6.1 vs 26.2 ± 6.3 [p = NS]; 24.1 ± 5.3 vs 23.5 ± 5.7 [p = NS]; 26.4 ± 5.7 vs 26.7 ± 6.1 [p = NS]). The sensitivity, specificity, and accuracy of these ST-T changes for detecting residual myocardial viability and ischemia documented by DSE in all patients were 50%, 53%, and 51% (for viability), and 47%, 48%, and 47% (for ischemia), respectively. The sensitivity, specificity, and accuracy of these ST-T changes for detecting a reversible perfusion defect documented by thallium-201 single-photon emission computed tomography were 51%, 54%, and 52%, respectively. In conclusion, dobutamine-induced ST elevation and/or T-wave pseudonormalization is associated with poor resting left ventricular function. These ST-T changes are not associated with residual myocardial ischemia and viability in the infarct area. Therefore, these electrocardiographic changes alone cannot be reliably considered as distinctive markers in formulating the therapeutic strategy of coronary intervention.

ST-segment elevation during dobutamine stress testing predicts functional recovery after acute myocardial infarction

Objectives The aims of this study were (1) to assess the relation between ST-segment elevation and wall motion response occurring during dobutamine testing and (2) to evaluate the usefulness of stress-induced ST-segment elevation for predicting functional recovery after acute myocardial infarction. Background Clinical significance of stress-induced ST-segment elevation after acute myocardial infarction remains controversial. According to previous studies, it may reflect a larger infarcted area, depressed left ventricular function, left ventricular aneurysm, stress-induced dyskinesia, residual myocardial ischemia, or viability in the affected region. Whether transient ST-segment elevation occurring during dobutamine testing may predict functional recovery is unknown. Methods and Results We studied 38 patients who underwent dobutamine stress testing early (5 ± 2 days) after a first acute myocardial infarction. Dobutamine was infused at increasing doses from 5 to a maximum of 40 μg/kg per minute, with the addition of up to 1 mg of atropine if the target rate could not be reached by dobutamine alone. Twelve-lead electrocardiography and cross-sectional echocardiography were continuously monitored throughout the test. Dobutamine-induced ST-segment elevation was defined as a new or worsening ≥1 mm elevation, 80 ms after J point, in ≥2 infarct-related leads. Quantitative angiography was available in all patients before hospital discharge. Follow-up resting echocardiography was recorded in all patients 12 to 18 months after the acute event. ST-segment elevation was observed in 20 of the 38 patients. There were no significant differences between patients with and those without dobutamine-induced ST-segment elevation in age, site of infarction, peak level of total creatine kinase enzyme, and use of thrombolytic therapy, angioplasty, or both. Persistent akinesis without change during dobutamine stress testing was more frequently observed in patients without ST elevation ( P < .05). A biphasic response during dobutamine testing was more frequently observed in patients with ST-segment elevation ( P = .01). Multivariate analysis selected 2 independent variables associated with ST-segment elevation: a biphasic response during dobutamine stress (chi-square = 7.3; P = .007) and the minimal lumen diameter of the infarct-related vessel at quantitative angiography (chi-square = 5.5; P < .02). Functional recovery was demonstrated in 26 patients. Sensitivity of ST-segment elevation for the prediction of functional recovery was 69%, specificity 83%, positive predictive value 90%, and accuracy 74%. Two independent variables predicting functional recovery were selected: dobutamine-induced ST-segment elevation (chi-square = 9.1; P = .003) and a biphasic response during stress (chi-square = 6.15; P = .013). Conclusions Dobutamine-induced ST-segment elevation in the infarct-related leads is an ancillary sign of viable myocardium in jeopardy. It has a high specificity and an acceptable sensitivity for the prediction of functional recovery after acute myocardial infarction. (Am Heart J 1999;137:500-11.)

Early infarct artery collateral flow does not improve long-term survival following thrombolytic therapy for acute myocardial infarction

It is known that acutely developed collaterals can prevent the onset of acute myocardial infarction (AMI) in the presence of a total coronary occlusion. However, there still is controversy concerning long-term follow-up of coronary collateral circulation to the infarct-related artery. In this study we analyze the prognostic role of collateral flow (degrees 0 to 3) as well as anterograde flow (degrees 0 to 3) in patients with AMI treated with thrombolytic therapy. Four hundred twenty-two patients (median age 57 years, 355 men) with AMI were treated with intravenous streptokinase and followed prospectively for up to 8 years. At the end of the study period, patients with collateral coronary flow 3 (n = 30) and those with flow <3 (n = 392) at in-hospital coronary arteriography had survival rates of 66% and 85%, respectively (p <0.12). Meanwhile, patients with coronary anterograde flow 3 (n = 189) and those with flow <3 (n = 233) had survival rates of 89% and 80%, respectively (p <0.04). By censored regression analysis, a negative correlation was found between coronary collateral flow degree and survival (p = 0.0498) and, inversely, a positive correlation was found between coronary anterograde flow degree and survival (p = 0.0053). By Cox multivariate analysis, the following variables showed significant correlations with long-term survival: global left ventricular ejection fraction (p = 0.0003), anterograde flow degree (p = 0.0006), collateral flow degree (negative correlation, p = 0.0179), and medical treatment (negative correlation, p = 0.0464). Thus, patients treated with intravenous streptokinase during AMI and with adequate coronary collateral circulation had a worse prognosis than those who developed adequate anterograde flow, probably because of residual myocardial ischemia. Such patients may benefit from coronary revascularization (angioplasty or surgery) to restore anterograde blood flow and minimize myocardium at risk.

¿Ectasia coronaria aterosclerótica o síndrome linfomucocutáneo del adulto (enfermedad de Kawasaki)?

We report the case of a 42-year-old man, who was admitted to hospital with an inferior myocardial infarction. He was treated with tissue plasminogen activator without complications in the acute phase. The stress testing performed before discharge showed residual myocardial ischemia. A catheterization study was indicated. The coronary angiogram demonstrated diffuse three vessel coronary artery aneurysmal disease. Two years before the patient had an aneurysm of the right iliac artery being operated on. The differential diagnosis of adult aneurysmal coronary disease is discussed with emphasis on Kawasaki's disease and atherosclerotic coronary artery ectasia.

Complex stenosis morphology predicts late reocclusion during follow-up after myocardial infarction in patients with patent infarct–related coronary arteries

Background Whether angiographic morphology of infarct-related residual stenoses continues to affect prognosis after discharge is not known. Methods We studied 175 patients after their myocardial infarction who required nonurgent coronary angioplasty for residual myocardial ischemia. The findings at diagnostic coronary angiography were compared with those before angioplasty (mean of 7 months later). Infarct-related stenoses were classified as complex or smooth. Stenosis progression was defined as >0.5 mm diameter reduction. Results One hundred twenty-one (69%) infarct-related stenoses were complex. At restudy, total occlusion was found in 41 (35%) of the infarct-related complex stenoses compared with 7 (13%) smooth stenoses ( P = .001). Reocclusion occurred in 16 (55%) of 29 complex infarct-related stenoses with thrombus, compared with 25 (28%) of 88 without thrombus ( P = .01). During follow-up, 46 patients (26%) had cardiac events. Of these, 70% had complex lesions at study entry compared with 30% smooth ( P < .05). Conclusions Residual angiographically complex stenoses after an uncomplicated myocardial infarction are associated with a greater risk of reocclusion and may predispose to coronary events at follow-up. (Am Heart J 1998;136:877-83.)

The Association Between Residual Myocardial Ischemia and Heart Rate Variability Early After Acute Myocardial Infarction

BackgroundResidual myocardial ischemia and decreased heart rate variability (HRV) are common findings during the acute phase of acute myocardial infarction. Both signs have been associated with a poor prognosis. The present study investigated the association between residual myocardial ischemia and HRV in the early phase after AMI.Patients and MethodsSeventy‐four patients were monitored with ambulatory electrocardiography during 23 ± 1 hours, 4 ± 1 days after AMI. In addition, 24 healthy individuals (controls) with similar age and gender were also monitored. HRV was computed in time and frequency domains. Residual myocardial ischemia was defined as the presence of ST‐segment depression during ambulatory electrocardiography, defined as a 0.1 mV horizontal or downsloping ST‐segment deviation from the reference level, elapsing 1 minute or longer, measured 80 ms after the J point.ResultsResidual myocardial ischemia was found in 22 (30%) patients. Some time‐domain and all frequency‐domain measures of HRV were lower in patients showing residual myocardial ischemia compared with those without residual myocardial ischemia. All time‐ and frequency‐domain measures of HRV were higher in controls compared with patients with residual myocardial ischemia. Only SDNN and low frequency band values were lower in patients without residual myocardial ischemia compared with healthy controls. Both residual myocardial ischemia and a decreased HRV were associated with poor in‐hospital outcome.ConclusionsPatients showing residual myocardial ischemia during ambulatory electrocardiography performed early after AMI had lower values of HRV compared with those without residual myocardial ischemia. The causality between these findings are not still defined and deserve further research.

Myocardial ischaemia un-masked by transesophageal atrial pacing combined with two-dimensional transthoracic echocardiography in a pediatric patient: a case report

We describe a case of a child operated on for an anomalous origin of the left coronary artery from the pulmonary artery and proximal hypoplasia of the anomalous coronary, in whom residual inducible myocardial ischaemia was detected by means of transesophageal atrial pacing combined with transthoracic echocardiography.

Use of the right gastroepiploic artery as a coronary artery bypass graft in 307 patients

From October 1988 to October 1995 the right gastroepiploic artery was used as a conduit for coronary surgery in 307 patients. Their average age was 56.5 years (range 25–75) and 274 patients (89%) were male. Twenty-six cases (8.5%) were re-operations and 58 patients (19%) were operated upon on an urgent or semi-urgent basis. Target coronary vessels were the right coronary artery and its branches in 280 cases (91.4%), the circumflex artery in 25 cases (8%) and the left anterior descending artery in two cases. The right gastroepiploic artery was used as an in situ graft in 303 cases (98.7%) and as a free graft in 4 (1.3%). A total of 291 patients (94.8%) also received at least one mammary artery graft: both mammary arteries were used in 167 patients (54.4%). An average of 3.6 distal anastomoses were made per patient, three of them with arterial grafts. Eleven (3.2%) right gastroepiploic artery grafts were doubled with saphenous vein intraoperatively because of persistent myocardial ischemia. In-hospital mortality was 1.6% (five patients). Perioperative myocardial infarction occurred in twelve patients (3.9%). Follow-up now averages 26 months (range 6–88). There have been five late deaths (1.6%). A total of 265 (89.2%) patients are angina free. Of the total, 145 patients have been investigated with a maximal-stress test coupled with scintigraphy: residual myocardial ischemia was found in 10 patients, right gastroepiploic artery was related in three. Ninety-six patients have undergone angiographic restudy at a mean of 12 months (range 8–88) postoperatively. Patency of the right gastroepiploic artery grafts was 91.8%. This study confirms that the right gastroepiploic artery can be used as a conduit for coronary artery bypass surgery with minimal mortality or morbidity. Mid-term patency rates and clinical outcome are encouraging.

The Effect of Ischemic Preconditioning on Patients Who Experienced Angina Pectoris Immediately before Acute Myocardial Infarction

Background and Objectives:Ischemic preconditioning (IP has been shown to reduce the infarct size and severity of arrhythmia in a post-ischemic reperfused heart. Angina before myocardial infarction reflects brief episodes of myocardial ischemia and may be a marker of ischemic preconditioning. We studied the effect of a history of previous angina on early outcomes (infarct size, left ventricular (LV function and residual myocardial ischemia for patients with acute myocardial infarction (AMI after thrombolytic therapy. Materials and Method:We examined prospectively 58 consecutive patients who had AMI and arrived hospital within 6 hours after chest pain developed. IP was defined as prodromal angina within 24 hours before myocardial infarction. Patients were divided 2 groups:Group Ⅰ (Gr Ⅰ, 30 cases without IP, Group Ⅱ (Gr Ⅱ, 28 cases with IP. Thrombolytic therapy was done 23 cases (77% and 21 cases (75% respectively in each groups. Thereafter, electrocardiographic findings, infarct size on the basis of peak creatine kinase, LV function on the 2-D echoc- ardiographic findings, recurrent myocardial ischemia were examined between 2 groups. Results:In predisc- harge 2-D echocardio-graphic findings, LV dilatation and normal regional wall motion did not differ between two groups. But, there were significantly smaller creatine kinase (CK-determined infarct size in Gr Ⅱ than that in Gr Ⅰ (peak CK level, Gr Ⅰ:1566.3±960.0 IU/L vs Gr Ⅱ:1066.9±773.2;p<0.05. The time interval between the onset of infarction and peak CK level was shorter in Gr Ⅱ than that in Gr Ⅰ (Gr Ⅰ:18.3±8.3 vs Gr Ⅱ:10.7±3.4 hours;p<0.001. There were significantly more common incidences of residual myoca- rdial ischemia in Gr Ⅱ (Gr Ⅰ:26.7% vs Gr Ⅱ:60.7%;p<0.01. Conclusion:Patients with a history of prodromal angina preceding myocardial infarction had small infarct size and earlier reperfusion of infarct related artery. However, there were significantly more common residual myocardial ischemia in these patients and a trend toward re-infarction on same previous infarction sites. (Korean Circulation J 1998;28(10 :1677-1684

Occurrence of Sustained Increase in QT Dispersion Following Exercise in Patients With Residual Myocardial Ischemia After Healing of Anterior Wall Myocardial Infarction

Our objective was to evaluate the effect of exercise on QT dispersion over the next 3 hours, as seen on a standard 12-lead electrocardiogram in patients with healed myocardial infarction with or without residual ischemia. We measured QT and QTc dispersion before, immediately after, and 1 and 2 hours after symptom-limited, dynamic treadmill exercise tests in 28 patients with healed anterior wall myocardial infarction with (group I, n = 18) and without (group II, n = 10) residual ischemia. The same protocol was followed in 5 group I patients after successful performance of coronary angioplasty. QT and QTc dispersion did not change immediately after exercise in group II. These parameters increased in group I (QT dispersion at rest [mean ± SD] 57 ± 22 ms, and after exercise 87 ± 27 ms; QTc dispersion at rest 62 ± 25 ms, and after exercise 114 ± 36 ms). The increases in QT and QTc dispersion were sustained for at least 2 hours. After a successful coronary angioplasty in 5 patients, these parameters no longer increased with exercise. Thus, QT dispersion increased for at least 2 hours after exercise in patients who had residual ischemia after healing of myocardial infarction. Data obtained in 5 of these patients after coronary angioplasty support the idea that residual ischemia plays a key role in the sustained increase in QT dispersion after exercise.

Significance of ST-segment elevation during dobutamine-stress echocardiography in patients with acute myocardial infarction treated with thrombolysis.

Stress-induced ST-segment elevation in patients with recent myocardial infarction treated with thrombolysis has not been extensively investigated. According to the results of previous studies it may represent residual myocardial ischaemia or dyskinesia in the infarcted region. The aim of the study was to analyse the significance of dobutamine-induced ST-segment elevation in the infarcted area in a consecutive group of patients (n = 42, 41 men, mean age 53 +/- 7 years) with a first acute myocardial infarction treated with thrombolysis within 6 h from symptoms onset. All patients underwent dobutamine-stress echocardiography (up to 40 micrograms.kg-1.min-1 + atropine) 7 +/- 3 days from the acute event and coronary arteriography within 1 month from the test. Significant ST-segment elevation was defined as a shift > or = 1 mm during dobutamine compared to baseline in at least two contiguous infarct-related leads; a correlation was made between the site of ST-segment elevation and wall motion changes during dobutamine. Dobutamine-induced ST-segment elevation in 23/42 (55%) patients (group 1) while no changes were observed in 19/23 (45%) patients (group 2). Compared to group 2, group 1 patients showed a higher asynergy score index (1.72 +/- 0.24 vs 1.50 +/- 0.32, P < 0.02) and a higher number of asynergic segments (5.04 +/- 1.9 vs 4.11 +/- 1.8), at baseline, a higher incidence of baseline and/or stress-induced dyskinesia (39 vs 10%, P < 0.05) in the infarct-related region and a higher percentage of occluded infarct-related arteries (48 vs 0%, P < 0.001). In the 42 patients studied, a significant correlation was found between baseline ST-segment elevation and baseline asynergy score index (RS = 0.56, P < 0.001) and between ST-segment elevation and asynergy score index at peak stress (RS = 0.55, P < 0.001). The incidence of reversible wall motion abnormalities indicative of myocardial viability and residual myocardial ischaemia was similar in the two groups (87 vs 84% and 74 vs 68%, respectively), while the number of segments with irreversible akinesia indicative of myocardial necrosis was higher in group 1 compared to group 2 (1.5 +/- 1.4 vs 0.9 +/- 1.4). Among the 23 patients of group 1 with dobutamine-induced ST-segment elevation, six had no reversible wall motion abnormalities indicative of myocardial ischaemia; of the 17 patients with myocardial ischaemia, 11 had > or = 50% and six had < or = 50% of basally asynergic segments showing reversible wall motion abnormalities. In patients with recent thrombolyzed myocardial infarction dobutamine-induced ST-segment elevation is associated with a larger akinetic area in basal conditions and either with reversible wall motion abnormalities indicative of myocardial ischaemia or with irreversible or minimally reversible wall motion abnormalities in the infarct area during the test. Thus, dobutamine echocardiography provides useful information for the interpretation of stress-induced ST-segment elevation and clinical management of these patients.

Role of adenosine thallium-201 tomography for defining long-term risk in patients after acute myocardial infarction

This study prospectively evaluated whether early assessment with adenosine thallium-201 tomography could better refine risk stratification on the basis of absolute extent of myocardial ischemia in postinfarction patients in clinically stable condition. Postinfarction patients are at increased risk for subsequent cardiac events. However, identifying high risk patients among those with residual myocardial ischemia is suboptimal. All 146 patients enrolled underwent assessment of left ventricular function and had adenosine tomography performed early (mean [+/- SD] 5 +/- 3 days) after infarction. Excluded from analysis were 51 patients with revascularization after scintigraphy and 3 lost to follow-up. Statistical risk models were therefore generated from the remaining 92 patients. Cardiac events occurred in 30 (33%) of 92 patients over 15.7 +/- 4.9 months. Univariate predictors of all events were quantified perfusion defect size (p < 0.0001), absolute extent of left ventricular ischemia (p < 0.000001) and ejection fraction (p < 0.0001). Risk was best predicted by Cox analysis on the basis of 1) absolute extent of ischemia and ejection fraction (chi-square 24.6); 2) percent infarct zone ischemia and ejection fraction (chi-square 24.4); or 3) total perfusion defect size and percent infarct zone ischemia (chi-square 18.9). The variables that predicted all cardiac events were equally powerful at predicting only death and nonfatal reinfarction. Death was best predicted by total perfusion defect size. Risk analysis of individual patients early after infarction is feasible on the basis of the quantified extent of scintigraphic ischemia and severity of left ventricular dysfunction.

Acute Myocardial Infarction: Risk Stratification in the Thrombolytic Era

Acute Myocardial Infarction: Risk Stratification in the Thrombolytic Era

Role of ischemia in postinfarction heart failure: Hypothetical considerations based on use of verapamil in the DAVIT II study

Based on a retrospective analysis of the DAVIT II database, we attempted to propose subgroups of post-infarction patients with heart failure, who might benefit or not benefit from antiischemic medical intervention. In DAVIT II, patients were randomized in a double-blind fashion to either verapamil 360 mg/day or placebo in the second week after the infarct and followed up to 18 months. The endpoint was the first major event; that is, death or reinfarction. In patients with heart failure but no ischemia, the event rate was 17.6% in the verapamil-treated patients and 16.5% in the placebo group (hazard verapamil: 1.01; 95% CL: 0.57, 1.79). In patients with both heart failure and residual ischemia, the event rate was 11.3% and 17.8% in the verapamil and placebo groups, respectively (hazard verapamil: 0.60; 95% CL: 0.24, 1.52). Although the latter reduction in major events was not statistically significant, we propose, in accordance with other studies, that in postinfarction patients with both heart failure and residual myocardial ischemia, the harmful negative inotropic effects of antiischemic drugs might be outweighed by their antiischemic effects, by means of which the prognosis might be improved. Patients without ischemia but with heart failure may, however, be at a disadvantage from such treatment.

Evidence of Residual Ischaemia: Real Danger or Myth?

The extent and severity of residual myocardial ischaemia are well-known as major determinants of mortality after myocardial infarction, and non-invasive assessment of these parameters still plays a critical role in the management of patients. Most of the published data on this topic derive from observations collected before the widespread use of thrombolysis. The results of large multicentre trials assessing the most appropriate therapies after thrombolysis have shown that the more conservative strategy of reserving catheterization and revascularization for patients with recurrent spontaneous or induced ischaemia may be the best approach. Sophisticated techniques to detect more accurately the residual ischaemic burden after infarction have been suggested that would have a major impact on clinical decision making and on the cost of health care. The relative influence of residual ischaemic on the prognosis after myocardial infarction, however, has recently been questioned. The relative risk associated with residual ischaemia seems to be low compared with other predictors of mortality. The progression of coronary artery disease is variable and highly unpredictable, and this may be a major limitation of our ability to predict further ischaemic events.

Dipyridamole echocardiography evaluation of acute inferior myocardial infarction with concomitant anterior ST segment depression.

The significance of anterior ST segment depression in inferior acute myocardial infarction (AMI) remains controversial. The aim of this study was to relate precordial ST segment depression to the topography of residual myocardial ischaemia, with myocardial mapping of the asynergic area and coronary anatomy. Twenty-five patients with first inferior AMI (15 patients with anterior ST segment depression: group A and 10 patients without anterior ST segment shift: group B), all underwent: (1) electrocardiographic evaluation on admission to the Coronary Care Unit and at 24 h intervals thereafter; (2) 2D-echocardiographic study within 3 h of CCU admission; (3) dipyridamole echocardiographic test (DET) (doses of dipyridamole up to 0.84 mg.kg-1 i.v. over 10 min) 4 days after AMI; (4) coronary arteriography within 14 days from AMI. To assess regional left ventricular wall motion, a 16 segment model was used and a wall motion score index (WMSI) was derived. The results of DET were correlated to the anatomy of the infarct-related vessel. Compared to group B, group A patients showed a significantly greater maximal ST segment elevation in inferior limb leads (lead III: 3.9 +/- 1.9 mm vs 2.2 +/- 1.1 mm, P < 0.05; aVF: 3.5 +/- 1.3 mm vs 1.7 +/- 0.8 mm, P < 0.001). Group A patients showed greater WMSI (1.35 +/- 0.22 vs 1.17 +/- 0.12, P < 0.05), with more frequent postero-lateral wall involvement (72% vs 20%, P < 0.05). No patient of either group showed asynergy of the anterior, anterolateral or anteroseptal segments. No differences in the distribution of coronary artery disease were observed.(ABSTRACT TRUNCATED AT 250 WORDS)