Q-wave Acute Myocardial Infarction Research Articles

New-onset angina preceding acute myocardial infarction is associated with improved contractile recovery after thrombolysis.

Ischaemic preconditioning reduces myocardial infarct size in animal models. Clinical data suggest that episodes of angina immediately before acute myocardial infarction may be associated with smaller infarct size in man. However, it is unclear whether ischaemic episodes preceding acute myocardial infarction also affect contractile recovery in patients. In this study we investigated the recovery of regional myocardial function after thrombolysis in two groups of patients at their first Q-wave acute myocardial infarction; in one group (n = 42) myocardial infarction occurred unheralded, whereas patients of the second group (n = 48) had experienced new-onset angina in the 48 h that preceded infarction. Echocardiographic analysis of myocardial regional function in the infarct area was done at 2, 24 and 72 h after thrombolysis, and at 1 week, and 1 and 3 months follow-up. Peak level of MB-creatine kinase was significantly lower in patients with new-onset angina (96 +/- 47 as compared with 221 +/- 108 IU.l-1, P < 0.01), as was the area under the MB-creatine kinase curve (1321 +/- 876 as compared to 3879 +/- 1555 U.l-1/36 h, P < 0.01). Hypokinetic segments were fewer in patients with pre-infarction angina. Similarly, wall motion score improved significantly earlier in patients who had new-onset angina before acute myocardial infarction. Thus, contractile recovery was more rapid in patients with previous angina than in those in whom infarction occurred unheralded. Complications during the in-hospital outcome and other variables considered during the 4-week follow-up were similar between groups. Patients who experienced new-onset angina before acute myocardial infarction showed better recovery of regional function after thrombolysis. Our study supports the hypothesis that brief periods of ischaemia immediately before myocardial infarction may precondition the human heart, thus improving contractile recovery.

The role of infarction-associated pericarditis on the occurrence of atrial fibrillation.

Transient atrial fibrillation is a relatively common arrhythmia in the early phase of acute Q-wave myocardial infarction. However, the role of infarction-associated pericarditis on the genesis of atrial fibrillation is controversial. This study was designed to examine the relative importance of infarction-associated pericarditis among other clinical variables on the genesis of transient atrial fibrillation in patients with acute myocardial infarction. Three hundred and ninety-eight patients with acute Q-wave myocardial infarction were examined carefully by means of auscultation, ECG, two-dimensional echocardiography and haemodynamic measurements. The diagnosis of pericarditis was made on the basis of pericardial rub detected during the first 3 days after admission. At least 0.5 mm of PQ-segment depression from a TP segment lasting more than 24 h in both limb and precordial leads was considered diagnostic of PQ-segment depression. Atrial fibrillation was present in 76 patients (19%). Sixteen (42%) of 38 patients with PQ-segment depression had atrial fibrillation, whereas 23 (30%) of 77 patients with pericardial rub had atrial fibrillation. Based on ten clinical variables, multivariate analysis was performed to determine the important variables related to the occurrence of atrial fibrillation. PQ-segment depression (chi-square = 4.10, P < 0.05) was selected with age (chi-square = 10.52, P < 0.005), the number of left ventricular segments with advanced asynergy (chi-square = 7.73, P < 0.01) and pericardial effusion (chi-square = 7.95, P < 0.005) as important factors related to atrial fibrillation. Patients with PQ-segment depression had a significantly higher pulmonary capillary wedge pressure than those without it. Among patients with infarction-associated pericarditis, those with PQ-segment depression represent atrial involvement associated with extensive myocardial damage and hence, PQ-segment depression is one of the clinical signs related to the occurrence of atrial fibrillation in acute Q-wave myocardial infarction.

Abstracts of Literature

Abstracts of Literature

Significance of Prolonged Left Ventricular Wall Motion Abnormalities After Exercise Echocardiography Following Non–Q-Wave Acute Myocardial Infarction

Exercise echocardiography was used to assess myocardial ischemia after non–Q-wave acute myocardial infarction in 40 consecutive patients. Resting parasternal long- and short-axis views and apical 4- and 2-chamber views were recorded, digitized, and stored. A maximal symptom-limited exercise test was performed within 21 days (mean 17.7 ± 3) using a cycle ergometer with continuous monitoring and the echocardiogram was repeated in the same views. Resting and exercise echocardiograms were then compared. Coronary angiography was performed in all patients within 21 days of exercise echocardiography. Stenosis in ≥50% of the lumen diameter was considered significant. Of the 40 patients studied, 29 (72%) had continuing angina and 11 (28%) had no angina. Eighteen patients (62%) with angina developed angina during exercise testing and 19 (65%) developed ST-segment depression. In patients without angina, 1 (9%) developed postexercise angina and 2 (18%) developed ST-segment depression. The mean wall motion score index after exercise increased from 1.2 ± 0.3 to 1.8 ± 0.4 in patients with continuing angina (p <0.001) and from 1.2 ± 0.3 to 1.4 ± 0.3 in patients without angina (p = NS). Prolonged wall motion abnormalities lasting >20 minutes persisted in ≥1 segment in 27 of 29 patients (93%) with angina or in 2 of 11 patients (18%) without angina (p <0.001). Patients with continued angina had predominantly 3-vessel coronary artery disease (22 of 29 [76%]) or 2-vessel disease (7 of 29 [24%]), and those without angina had 1-vessel disease (6 of 11 [55%]) or 2-vessel disease (4 of 11 [36%]). One patient had 3-vessel disease. The duration of wall motion abnormality demonstrated a significant relation to 2- and 3-vessel coronary artery disease (p <0.001). Thus, patients with non–Q-wave acute myocardial infarction had a high incidence of multivessel coronary disease not necessarily detected on routine exercise testing. There was also a significant incidence of prolonged wall motion abnormality.

Myocardial revascularisation in elderly patients with refractory or unstable angina and advanced coronary disease.

Elderly patients with ischaemic heart disease are often treated more conservatively and for longer than younger patients, but this strategy may result in subsequent invasive intervention of more advanced and higher risk coronary disease. We performed a retrospective analysis of 109 patients aged > or = 70 years (mean age 74 years, 66% men), who presented with angina refractory to maximal medical treatment or unstable angina over a 2-year period (1988-1990), to compare the relative risks and benefits of myocardial revascularisation [coronary artery bypass grafting (CABG) and percutaneous transluminal coronary angioplasty (PTCA)] in this higher-risk age group. Sixty patients underwent CABG and 49 patients PTCA. There were eight periprocedural deaths in total (six in the CABG group, and two in the PTCA group, P = 0.29). Six patients in the CABG group suffered a cerebrovascular accident (two fatal). Acute Q-wave myocardial infarction occurred in one patient in the CABG group and in two patients in the PTCA group. The length of hospital stay was longer for the CABG group (CABG group 11.4 +/- 5.4 days, range 7-30 days, PTCA group 7.4 +/- 7.6 days, range 1-39 days, P = 0.01). Outcome was assessed using the major cardiac event rate (MACE; i.e. the rate of death, myocardial infarction, repeat CABG or PTCA). The cumulative event-free survival in the CABG group in 1, 2 and 3 years was 87, 85 and 85%, respectively. In contrast, in the PTCA group it was 55, 48 and 48% (P = 0.0001). Age, sex, number of diseased vessels, degree of revascularisation and left ventricular function were not predictive of the recurrence of angina in both groups. Actuarial survival (total mortality, including perioperative mortality) was lower at 1 year in the CABG group due to the higher perioperative mortality, but similar in both groups after the second year (P = 0.62). Elderly patients with refractory or unstable angina who are revascularised surgically have a better long-term outcome (less frequent event rate of the composite end-point--myocardial infarction, revascularisation procedures and death) compared with those who are revascularised with PTCA. This benefit is been realised after the second year. Total mortality is similar in both groups after the second year. Therefore elderly patients who are fit for surgery should not be denied the benefits of CABG. PTCA may be regarded as a complementary and satisfactory treatment, especially for those whose life expectancy is limited to less than 2 years. The use of stents may improve outcome in the PTCA group and this needs to be evaluated.

Diagnostic and Prognostic Value of Dipyridamole and Dobutamine Stress Echocardiography in Patients With Q-Wave Acute Myocardial Infarction

The aim of this study was to compare dipyridamole and dobutamine stress echocardiography, performed early in patients with acute myocardial infarction (AMI) to evaluate residual ischemia, viability, and prognosis. Fifty patients (mean age 55 ± 9 years, 47 men, 3 women) with AMI, all treated with thrombolytic therapy, underwent standard dipyridamole and dobutamine tests, within the fifth day of the event. Wall motion score index and the 16 segments model were used to evaluate contractility. Forty-seven patients underwent coronary angiography within the tenth day of the event. The mean follow-up was 24 ± 12 months. No side effects occurred during both tests. Both dipyridamole and dobutamine tests were positive for ischemia, in 32 and 33 of 47 patients, respectively (sensitivity 73% and 75%; specificity 67% and 67%); these tests induced an improvement of contractility in 23 and 38 of 139 abnormal segments at baseline, respectively (sensitivity 52% and 86%; specificity 100% and 100%). Cardiac events occurred in 26 of 50 patients, 22 with a positive dipyridamole test and 21 with positive dobutamine test. Thus, both tests were feasible, safe, and useful to evaluate residual ischemia, viability, and prognosis. No significant differences were found in sensitivity and specificity between tests.

The 60 minutes myocardial infarction project. Treatment and clinical outcome of patients with acute myocardial infarction in Germany.

To describe patient characteristics, pre-hospital delay, treatment, complications and outcome in patients with acute myocardial infarction admitted to hospitals in Germany. The study was of prospective observational multicentre design. Those involved were consecutive patients with acute Q-wave myocardial infarction admitted within 96 h of onset of symptoms to 136 German hospitals between July 1992 and September 1994 (n = 14980, median age 66 (quartiles 57, 74) years, 68% male, 48% anterior wall infarction). Median pre-hospital delay was 170 (90, 475) min, with 17% arriving within the first hour and 61% within 4 h of onset of symptoms. The following patient groups had a short pre-hospital delay: males, those aged less than 65 years, those admitted at night or the weekend, those with a previous myocardial infarction, those in need of cardiopulmonary resuscitation, and those with a diagnostic first ECG. The first ECG was diagnostic in 67.6% of cases. Reperfusion therapy was used in 53%, with thrombolytic therapy in 51.6%. Median time from admission to initiation of treatment was 30 (20, 55) min. Respective rates of treatment with aspirin, nitrates, and beta-blockers were 81%, 83%, and 16%. Major complications were cerebral bleeding (0.4%), bleeding requiring transfusions (0.9%), left ventricular rupture (0.6%) and anaphylactic shock (0.1%). Median hospital stay was 20 (13, 26) days. In-hospital death rate was 17.2%. Increased hospital mortality was observed with female gender, an unknown or long pre-hospital delay, a diagnostic first ECG, anterior wall infarction, trauma or major operation within the last 14 days, renal insufficiency and malignoma. 'Real-life' hospital mortality is much higher than previously reported in clinical trials. To reduce hospital mortality, the efficacy of thrombolysis should be increased by shortening the pre-hospital delay, and the use of concomitant therapy, especially beta-blockers, should be increased.

C-reactive protein as a predictor of infarct expansion and cardiac rupture after a first Q-wave acute myocardial infarction.

Pump failure after acute myocardial infarction (AMI) can be predicted by several indices that estimate infarct size. However, there are few indices that predict infarct expansion and cardiac rupture. We focused on the prognostic significance of serum C-reactive protein (CRP) after AMI. Serum CRP levels were measured every 24 hours in 220 patients with a first Q-wave AMI. In-hospital complications, predischarge left ventriculographic findings, and long-term prognosis were assessed in relation to peak CRP levels. Peak levels of both CRP and creatine kinase (CK) were higher in patients with pump failure than in those without pump failure. In patients with cardiac rupture, peak CRP levels were higher than in those without rupture (P=.001); peak CK levels were not predictive. Higher CRP levels were found in patients with left ventricular aneurysm (P=.001 versus those without), aggravated heart failure (P=.03 versus those without), and cardiac death (P<.0001 versus survivors) during the first year after AMI. Multivariate analysis confirmed that an elevation of the peak CRP level > or = 20 mg/dL was an independent predictor of cardiac rupture (relative risk, 4.72; P=.004), left ventricular aneurysmal formation (relative risk, 2.11; P=.03), and 1-year cardiac death (relative risk, 3.44; P<.0001). Cardiac rupture, left ventricular aneurysmal formation, and 1-year cardiac death were associated with an elevation of serum CRP early after AMI, suggesting that elevation of CRP levels after AMI may predict infarct expansion.

Relationship between rate-corrected QT interval and wall motion abnormalities in the setting of acute myocardial infarction

We studied 108 patients (73 men and 35 women, mean age of 63.1±11.2 years) with Q-wave acute myocardial infarction (anterior −52, inferior −41, and combined anteroinferior −15) 4 days after infarct onset to determine whether any correlation exists between rate-corrected QT interval (QTc) and functional infarct size, expressed as wall motion index. QTc was calculated by Hodges' linear algorithm [QT+(1.75×heart rate−60)]. Wall motion index was determined using a 16-segments model, as recommended by the American Society of Echocardiography. Wall motion index was significantly higher in anterior and in combined infarctions. QTc was shortest in inferior infarction. There was a statistically significant overall correlation between wall motion index and QTc (r=0.83, p<0.001). The relationship was weakest in inferior infarction. In conclusion, prolonged QTc may be implicated as an additional marker of left ventricular dysfunction in patients with acute anterior and combined anteroinferior myocardial infarction.

Incidence and Natural History of Left Ventricular Thrombus Following Anterior Wall Acute Myocardial Infarction

Previous studies have reported left ventricular (LV) thrombus in 20% to 56% of patients after anterior wall acute myocardial infarction (AMI). The Healing and Early Afterload Reducing Therapy (HEART) study was a prospective study comparing effects of early (24 hours) or delayed (14 days) initiation of ramipril, an angiotensin-converting enzyme inhibitor, on LV function after anterior wall AMI. This ancillary study assessed prevalence of LV thrombus. Two-dimensional echocardiography was performed on days 1, 14, and 90 after myocardial infarction. The cohort consisted of 309 patients. Q-wave anterior wall AMI occurred in 78%; 87% received reperfusion therapy. The prevalence of LV thrombus was 2 of 309 (0.6%) at day 1, 11 of 295 (3.7%) at day 14, and 7 of 283 (2.5%) at day 90. One patient had thrombus at 2 examinations. The day 1 echocardiogram was not correlated with thrombus development. LV size increased more in patients with thrombus than in those without thrombus. Patients with thrombus had more wall motion abnormality after day 1 than patients without thrombus (p = 0.03). Thus, the current prevalence of LV thrombus in anterior wall AMI is lower than previously reported, possibly due to changes in AMI management. Preservation of LV function is likely to be an important mechanism. Most thrombi are seen by 2 weeks after AMI. Resolution documented by echocardiography is frequent.

Management of Unstable Angina Pectoris and Non-Q-Wave Acute Myocardial Infarction in the United States and Canada (The TIMI III Registry)

Management of Q-wave acute myocardial infarction (AMI) has been shown to differ between the United States and Canada, with more catheterization and revascularization procedures performed in the United States, but with little or no apparent difference in clinical outcomes. No previous studies have evaluated management differences for the acute coronary syndromes of unstable angina pectoris and non-Q-wave AMI. We therefore compared treatments and outcomes between 14 United States and 4 Canadian tertiary care centers participating in an observational registry of all consecutive admissions for unstable angina or non-Q-wave AMI between 1990 and 1993. A random, stratified sample was selected for detailed assessment and follow-up. There were 1,733 patients enrolled in United States centers and 642 in Canadian ones. In United States centers patients were less likely to receive intravenous nitroglycerin, heparin, β blockers, calcium antagonists, or ≥2 anti-ischemic agents. Coronary arteriography during index hospitalization was equally frequent in both countries (63.4% vs 66.9%, p = 0.781), but at 6 weeks and 1 year coronary arteriography was slightly less frequent in the United States patients. Revascularization by coronary angioplasty or bypass surgery was equivalent at 6 weeks and 1 year; however, there were trends toward less angioplasty and more bypass surgery in the United States than in Canada. Patients at United States centers stayed in the hospital fewer days than patients at Canadian centers (mean 8.2 vs 12.1 days, p <0.001). Death or AMI by 6 weeks was not different (4.8% vs 4.4%, p = 0.633), nor was it different at 1 year (10.0% vs 10.2%, p = 0.836). The combined outcome of death, AMI, or recurrent ischemia was more common in United States than in Canadian patients at 6 weeks (18.4% vs 13.9%, p = 0.004). Our findings indicate that United States physicians and hospitals did not consistently utilize more resources and were not more aggressive than their Canadian counterparts when treating acute coronary syndromes during this period.The TIMI III Registry prospectively studied hospital admissions for unstable angina pectoris and non-Q-wave myocardial infarction at 18 tertiary care institutions in the United States and Canada. Results suggest that physicians at Canadian hospitals are equally aggressive as United States physicians in management of these acute coronary syndromes.

Frequency of Pericardial Friction Rub (“Pericarditis”) After Direct Percutaneous Transluminal Coronary Angioplasty in Q-Wave Acute Myocardial Infarction

The clinical significance of infarct-associated pericarditis was examined in 201 consecutive patients with acute Q-wave myocardial infarction with successful direct percutaneous transluminal angioplasty. A pericardial rub was a reliable clinical sign of extensive myocardial damage in patients with direct angioplasty.

Aprotinin in aortic surgery requiring profound hypothermia and circulatory arrest.

The use of aprotinin in cardiac surgery to improve haemostasis and reduce blood loss particularly in patient groups at increased risk of bleeding is well established. Previous retrospective studies in profound hypothermic surgery have highlighted concerns that in this circumstances aprotinin may paradoxically cause increased bleeding and intravascular thrombosis. We therefore adopted a modified protocol for administering aprotinin, which was not started until cardiopulmonary bypass had been reinstituted after circulatory arrest. Between April 1993 and June 1995, 45 patients underwent 46 thoracic aortic procedures which required hypothermic circulatory arrest; 25 of these were emergencies. All of these patients received aprotinin. There were five deaths (10.8%) in hospital. Two patients with preoperative oliguric renal failure required postoperative dialysis, and a further six (13%) developed transient renal dysfunction with complete recovery. Two patients suffered postoperative stroke; one from embolisation of a severely diseased aorta, while the other had signs of an acute evolving stroke before surgery. None of the patients suffered acute Q-wave perioperative myocardial infarction. The mean blood loss was 575 ml in the first 12 h, with a mean postoperative transfusion requirement of 1 U blood. We cannot implicate aprotinin in increased postoperative blood loss, renal dysfunction or mortality when used with hypothermic circulatory arrest according to this protocol. Elucidating the role of aprotinin in hypothermic circulatory arrest requires a randomised prospective study.

Primary Angioplasty Versus Thrombolysis in the Treatment of Acute Myocardial Infarction

This study investigates the hypothesis if primary angioplasty is superior to intravenous thrombolysis in the treatment of acute myocardial infarction (AMI). Small prospective randomized studies did not demonstrate a significant benefit regarding total mortality. A total of 14,980 patients with AMI were registered by “The 60-Minutes Myocardial Infarction Project,” a prospective multicenter observational study: 210 of these patients were treated with primary angioplasty. A matched pair analysis comparing 1 primary angioplasty patient with 3 intravenous thrombolysis patients could be performed in 156 primary angioplasty patients. Criteria for matching were age, sex, location of AMI, systolic blood pressure, previous AMI, and prehospital delay. Patients with a bundle branch block or requiring resuscitation were excluded from analysis. Because of matching, both groups showed similar baseline characteristics. Patients with primary angioplasty had more relative contraindications for thrombolysis (ulcers: 10.3% vs 2.3%, recent intramuscular injections: 6.4% vs 1.6%, recent surgical interventions: 5.1% vs 1.1%, central punctures: 9% vs 3.9%). There was a tendency toward less combined adverse events in the primary angioplasty group (3.2% vs 5.7%, odds ratio [OR] = 0.55, 95% confidence interval [CI] = 0.21 to 1.44). In-hospital mortality rates in the primary angioplasty group and thrombolysis group were 4.3% and 10.3%, respectively (OR = 0.39, 95% CI = 0.17 to 0.92). The difference in mortality could already be demonstrated within the first 48 hours with 1.9% versus 5.3% deaths (OR = 0.35, 95% CI = 0.11 to 1.14). Thus this study indicates a superiority of primary angioplasty in comparison to intravenous thrombolysis in AMI even in a clinical routine setting, with a reduction of hospital mortality of about 60%.In 156 patients receiving primary angioplasty for acute Q-wave myocardial infarction, a matched pair analysis was performed comparing 1 primary angioplasty patient with 3 intravenous thrombolysis patients. In-hospital mortality rates in the primary angioplasty and thrombolysis groups were 4.3% and 10.3%, respectively (odds ratio = 0.39, 95% confidence interval = 0.17 to 0.92), indicating a superiority of primary angioplasty in the treatment of acute myocardial infarction.

The predictive value of the electrocardiographic pattern of acute Q-wave myocardial infarction for recurrent ischemia.

A total of 140 consecutive patients with acute Q-wave myocardial infarction was evaluated to assess the relationship between different electrocardiographic patterns of evolution and the incidence of recurrent ischemia within 10 days of infarction. Patients were allocated to three groups according to the electrocardiogram at 12 h after admission: Group A: ST elevation of < 2 mm and negative T waves (75 patients); Group B: ST elevation of > 2 mm and negative T waves (35 patients); Group C: ST elevation of > 2 mm and positive T waves (30 patients). Patients in Group C had more anterior wall infarctions (82%) than Group A (40%) or Group B (58%) (p = 0.0001). Peak creatine kinase levels were lower in Group A (782 +/- 115 IU) than in Groups B (1415 +/- 257 IU) and C (1501 +/- 287 IU) (p < 0.0001). The occurrence of post-infarction recurrent ischemia was more frequent in Group A (79.2%) than in Groups B (33.3%) and C (14.8%) (p < 0.0001). Patients in Group A had relatively smaller infarctions and a higher incidence of recurrent ischemia, whereas patients in Group C had larger infarctions and a lower incidence of recurrent ischemia. The electrocardiographic pattern 12 h after admission for acute myocardial infarction is helpful in identifying a subgroup at high risk of recurrent ischemia.

Effect of early enalapril therapy on left ventricular function and structure in acute myocardial infarction

Infarct expansion starts within hours to days after transmural myocardial injury. Previous echocardiographic and left ventriculographic studies demonstrated that angiotensin-converting enzyme (ACE) inhibitor therapy limits left ventricular dilatation, particularly in patients with anterior wall acute myocardial infarction (AMI) or impaired left ventricular function. Forty-three patients with an acute Q-wave AMI were randomized within 24 hours of symptom onset to intravenous enalaprilat (1 mg) or placebo. Patients were then given corresponding oral therapy and followed for 1 month. Predrug and 1-month gated blood pool scans were obtained in 32 patients to evaluate changes in cardiac volumes and ejection fraction. Twenty-three patients underwent magnetic resonance imaging at 1 month to evaluate left ventricular infarct expansion. Blood pressure decreased at 6 hours but returned to baseline in both groups after 1 month of therapy. The change in cardiac volumes from baseline to 1 month differed between the placebo (end-diastolic volume +16 ± 5 ml, end-systolic volume +8 ± 6 ml), and enalapril (end-diastolic volume −8 ± 9 ml and end-systolic volume −14 ± 7 ml) groups (p < 0.05 vs placebo). Global and infarct zone ejection fractions improved significantly at 1 month in the enalapril group (+6 ± 3% and 19 ± 5%, respectively) but did not change over 1 month in the placebo group. Infarct segment length and infarct expansion index by magnetic resonance imaging were significantly less in those treated with enalapril, suggesting less infarct expansion in this group. Thus, early administration of enalaprilat to patients presenting with a first Q-wave AMI prevents cardiac dilatation and infarct expansion.

Optimizing the Treatment of Unstable Angina.

Unstable angina and non--Q-wave myocardial infarction (MI) are at the center of the spectrum of myocardial ischemia, which ranges from stable angina to acute Q-wave MI. In addition to clinical evaluation, cardiac specific markers such as troponin T or I can assist in early diagnosis, triage, and risk stratification. Antithrombotic therapy with aspirin and heparin have been shown to improve the outcome of patients with acute ischemic syndromes. Thrombolytic therapy does not appear to be beneficial in these syndromes. Antiischemic therapy remains an important component of the overall therapy. A strategy of early coronary angiography and revascularization leads to a similar long-term outcome as compared with a more conservative strategy of revascularization for recurrent ischemia, but the early invasive strategy is more expeditious as a large number of conservatively treated patients have recurrent ischemia. At present, many new antithrombotic agents are under active investigation, with the hope that they will lead to further improvement in the clinical outcome of patients with acute ischemic syndromes.

Characteristics and prognostic importance of ST-segment elevation on Holter monitoring early after acute myocardial infarction

The correlation between episodes of ST-segment elevation on Holter monitoring, clinical characteristics, left ventricular function, exercise testing, and long-term prognosis was determined in 123 consecutive patients 55 ± 8 years old (mean ± SD) with a first acute myocardial infarction (AMI). During 36 hours of Holter recording 11 ± 5 days after AMI, 11 patients (9%) had 91 episodes of ST-segment elevation (group 1), whereas 112 patients had no such episodes (group 2). Most episodes of ST-segment elevation occurred in leads with pathologic Q waves or small, indistinct R waves. Large, anterior Q-wave AMIs were more prevalent in group 1 than in group 2, and in-hospital heart failure also occurred more frequently in group 1 patients (82% vs 23%; p < 0.0005). Regional and global left ventricular function was reduced in group 1 compared with group 2: ejection fraction 33 ± 11% vs 50 ± 11% (p = 0.0001). All episodes of ST-segment elevation were asymptomatic and did not correlate with different indicators of myocardial ischemia. Indeed, exercise-induced ST-segment depression was more prevalent in group 2 than in group 1: 57 vs 18% (p < 0.035). Over a mean of 5 years (range 4 to 6) of follow-up, an association between episodes of ST-segment elevation on Holter monitoring and (1) cardiac death (Kaplan-Meier analysis; p < 0.005), and (2) cardiac death and nonfatal reinfarction (Kaplan-Meier analysis; p < 0.025) was found. If, however, the symptomatic need for coronary revascularization was included as an end point, no association between episodes of ST-segment elevation and long-term outcome could be demonstrated (Kaplan-Meier analysis; p = NS).

Relation between myocardial infarction site and pain location in Q-wave acute myocardial infarction

Location, severity, duration, and time course of pain were assessed in 104 consecutive patients with either first or second, anterior or inferior Q-wave acute myocardial infarction (AMI). Pain severity was assessed using a visual analog scale. Pain location and radiation were similar in 48 patients with anterior and 56 patients with inferior wall AMI. Pain duration (6.1 ± 6.4 vs 6.5 ± 5.4 hours, p = NS) and severity (68 ± 21 vs 61 ± 21 mm, p = NS) were also similar. The pain was continuous in 34 patients with anterior (71%) and in 42 with inferior (75%) wall AMI. Among the 41 patients who did not receive thrombolytic therapy, 18 patients with continuous pain had a higher creatine kinase peak level than the remaining 23 patients with intermittent pain or preinfarction angina, or both (2,065 ± 1,017 vs 1,162 ± 994 IU, p <0.01). The incidence of gastrointestinal symptoms was slightly higher in patients with inferior than anterior wall AMI (70% vs 48%, p <0.05). Among 32 patients admitted with a second AMI, pain location was similar in 14 who had both infarcts in the same myocardial region, but was different in 12 of 18 (67%) who had a first and second infarct in different regions ( p <0.001). Thus, patients with anterior or inferior wall AMI experienced pain in similar body regions. However, in patients who presented with >1 AMI, different locations of the infarction pain were highly predictive of ischemia occurring in different myocardial regions. Finally, patients with preinfarction angina or intermittent pain tended to have smaller infarcts.

901-30 Relationship Between Function, Perfusion and Contractile Reserve Early After Myocardial Infarction: A Dynamic Magnetic Resonance and Stress Echocardiographic Study in Man

To assess the relationship between regional myocardial function, myocardial perfusion pattern and contractile reserve, 12 patients (age 53.5 ± 9.3 years; mean ± SD) were studied 4.5 ± 0.9 days after the occurrence of their first Q-wave acute myocardial infarction. Myocardial perfusion was evaluated by an ultrafast gradient echo sequence, implemented on a 0.5 T system for magnetic resonance imaging (MRI). During the acquisition of 64 consecutive, single slice, ECG triggered, diastolic, short axis images of the left ventricle a bolus of gadopentetate (0.05 mmol/kg) was injected intravenously. Six regions of interest (ROIs) were drawn on the left ventricle profile of the images and time-intensity curves were obtained. In each patient the time-intensity curve from a region with normal function was used as reference to cross-correlate curves from the other ROIs. A cross-correlation coefficient (CCC), which described the state of myocardial perfusion was obtained for each ROI ranging from 1 (normal perfusion pattern) to 0 (no perfusion). Regional contractile reserve was assessed by 2-D echocardiography at rest and following low dose (up to 10 mcg/kg/min) dobutamine infusion. Out of the 72 regions analysed, 44 segments had normal function and normal perfusion (CCC = 0.91 ± 0.13). The remaining 28 regions with resting dyssynergy showed a reduced perfusion (CCC = 0.61 ± 0.28; p &lt; 0.05 vs normal regions). Perfusion deficit was more marked in the 11 aki-dyskinetic regions than in the 17 hypokinetic regions (CCC = 0.35 ± 0.20 vs 0.77 ± 0.20; p &lt;0.05). Out of the 11 regions with severe dyssynergy (resting aki-dyskinesia) the 4 segments showing a functional improvement following dobutamine had a higher perfusion when compared to the 7 segments unresponsive to dobutamine (CCC = 0.54 ± 0.1 vs 0.24 ± 0.17; p &lt; 0.05). In conclusion, early after an acute myocardial infarction, the severity of the perfusion deficit in the infarcted regions tends to mirror the severity of the mechanical dysfunction. In regions with severe baseline dyssynergy, perfusion is lower when no contractile reserve can be elicited by dobutamine. The integration of dynamic MRI and low dose pharmacological stress-echo allows to explore non-invasively the relationship between function, myocardial perfusion pattern and contractile reserve in man.