Prognostic importance of delayed Q-wave evolution 3 to 24 hours after initiation of thrombolytic therapy for acute myocardial infarction

The timing of Q-wave evolution and its prognostic significance was studied in 201 patients who received thrombolytic therapy for a first acute myocardial infarction (AMI). One hundred forty-one patients (70%) had evidence of a Q-wave AMI within 3 hours of the initiation of thrombolytic therapy, 31 (16%) developed Q waves after 3 hours but before hospital discharge, and 29 (14%) were discharged with a non-Q-wave AMI. Laboratory indicators of myocardial damage and in-hospital morbidity and mortality were greater among patients with Q-wave AMIs than with non-Q-wave AMIs. When these indexes were examined with respect to the timing of Q-wave evolution, the prognosis of patients with delayed Q-wave development was similar to that of patients with non-Q-wave AMIs. Thus, compared to patients with early (less than or equal to 3 hours) Q-wave evolution, patients with delayed Q-wave evolution or with a non-Q-wave AMI had a smaller creatine kinase peak (mean 661 to 1,081 vs 1,251 to 1,541 IU; p = 0.005), better preservation of left ventricular function as measured by radionuclide ventriculography before discharge (mean +/- standard deviation 54 +/- 11% vs 47 +/- 13%; p less than 0.01), and a lower incidence of congestive heart failure at discharge (3 vs 15%; p = 0.02). In-hospital mortality was lower among patients with delayed Q-wave evolution or with a non-Q-wave AMI (5 of 141 vs 0 of 60; difference not significant).(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and prognostic significance of lung thallium uptake on rest imaging in acute myocardial infarction

Exercise-induced pulmonary uptake of thallium-201 in patients with ischemic heart disease is probably due to transient pulmonary edema and left ventricular failure induced by exercise. The significance of increased lung uptake of thallium-201 at rest after acute myocardial infarction (AMI) has not been described. Ninety-six patients admitted with chest pain for suspected AMI or unstable angina underwent thallium-201 imaging at rest. Using conventional diagnostic criteria, 62 had AMI, 12 had unstable angina and 22 had neither. Increased lung uptake of thallium-201 was present in 24 of the total 96 (25%) patients, 20 of the 62 (32%) patients with AMI and 4 of 34 (13%) patients with no evidence of infarction. In the AMI group, those with increased lung thallium-201 uptake had a higher mean +/- standard deviation segmental thallium-201 defect score (22 +/- 7 vs 12 +/- 8, p less than 0.0001), lower ejection fraction (35 +/- 14 vs 49 +/- 14%, p less than 0.002), higher peak creatine kinase levels (2,410 +/- 1,247 vs 1,496 +/- 1,228 IU/liter, p less than 0.01), higher wall motion abnormality score (25 +/- 13 vs 13 +/- 12, p less than 0.0001), increased incidence of clinical in-hospital heart failure (15 of 20 vs 7 of 42, p less than 0.0001) and higher short-term mortality (4 of 20 vs 1 of 42, p less than 0.02) compared to those without increased lung thallium-201 uptake.(ABSTRACT TRUNCATED AT 250 WORDS)     

Frequency and significance of late evolution of Q waves in patients with initial non-Q-wave acute myocardial infarction. Diltiazem Reinfarction Study Group

Serial 12-lead electrocardiogram and plasma creatine kinase (CK)-MB values from 544 patients with confirmed non-Q-wave acute myocardial infarction (AMI) were analyzed to define the rate of progression of non-Q-wave AMI to Q-wave AMI and to examine its relation to CK-MB evidence of extension. The baseline electrocardiogram was obtained 50 +/- 10 hours after AMI and compared with subsequent electrocardiograms at 48 and 72 hours after baseline record and at discharge. Plasma CK-MB was assayed every 12 hours after baseline. A total of 76 patients (14%) progressed to Q-wave AMI. Compared to the 468 patients who retained non-Q-wave AMI, those patients who evolved Q-wave AMI were more likely to exhibit ST elevation greater than or equal to 1.0 mm in greater than or equal to 2 infarct-related leads (49 vs 32%, p less than 0.005), higher peak CK values with the index AMI (754 +/- 625 vs 611 +/- 604 IU; p = 0.0018) and a greater incidence of CK-MB-confirmed extensions (18.5 vs 5.5%, p less than 0.0001). For those patients progressing to Q-wave AMI within 48 hours of baseline electrocardiogram, CK-MB extension occurred in 9.5% (4 of 42) versus 29.4% (10 of 34) of those who progressed after 48 hours (p = 0.0262). A distinct minority (14%) of patients with non-Q-wave AMI will develop Q waves before discharge. The progression to Q-wave AMI after initial non-Q-wave AMI appears to involve 2 different mechanisms: temporal lag in the electrocardiogram, and actual extension by quantitative CK-MB criteria.     

Short- and long-term prognostic importance of complete bundle-branch block complicating acute myocardial infarction

Among 1013 consecutive patients with acute myocardial infarction (AMI), 104 (10%) developed complete bundle-branch block (BBB). The clinical characteristics and the short- and long-term prognosis were similar in the 53 patients with right and the 51 patients with left BBB. Compared to the 909 patients without this conduction disturbance, these 104 patients were older (64 +/- 9 vs. 58 +/- 10 years, p less than 0.001), more frequently women (26 vs. 17%, p less than 0.05), had a larger infarct (peak CK 1672 +/- 1124 vs. 1356 +/- 1089 IU/l, p less than 0.001), more frequently anterior (60 vs. 37%, p less than 0.001). They had a higher incidence of Killip class greater than 1 (63 vs. 38%, p less than 0.001), pericarditis (40 vs. 23%, p less than 0.001), atrial fibrillation or flutter (22 vs. 12%, p less than 0.01), ventricular fibrillation (15 vs. 9%, p less than 0.05), and atrioventricular block (23 vs. 11%, p less than 0.001). Both hospital mortality (32 vs 10%, p less than 0.001) and 3-year posthospital mortality (37 vs. 18%, p less than 0.001) were much higher among patients with complete BBB. Transient BBB had the same deleterious prognosis as BBB persistent at discharge (mortality 33 vs. 39%, NS). The prognostic importance of BBB was more prominent during the first 6 months after infarction (mortality between 6 and 36 months: 18% with BBB vs. 11% without BBB, NS).     

Clinical significance and prognostic importance of left ventricular hypertrophy in non-Q-wave acute myocardial infarction

Left ventricular (LV) hypertrophy is known to be an independent risk factor for cardiac death, but its significance in non-Q-wave acute myocardial infarction (AMI) has not been assessed previously. In a randomized diltiazem-placebo-controlled therapeutic trial of non-Q-wave AMI confirmed by creatine kinase-MB (CK-MB), 126 of 544 patients (23%) exhibited LV hypertrophy using standard voltage criteria. Compared to patients without LV hypertrophy, patients with LV hypertrophy were significantly older (65 vs 60 years, p less than 0.0001) and had smaller peak adjusted CK levels (490 +/- 376 vs 666 +/- 726 IU/liter, p less than 0.001) than patients without LV hypertrophy. Patients with and without LV hypertrophy did not differ significantly in acute mortality during hospitalization, progression to Q waves, reinfarction by CK-MB criteria or angina associated with transient electrocardiographic changes. Compared with patients without LV hypertrophy, those patients with non-Q-wave AMI and LV hypertrophy had a 2-fold higher incidence of reinfarction (24 vs 12%, p less than 0.005) and death (19 vs 9%, p = 0.044) during the first year of follow-up. Multivariate regression analysis revealed that the relative risk of death and reinfarction during the initial year after AMI was increased by a factor of 1.7 and 2.1 among patients with LV hypertrophy, respectively. It was therefore concluded that, although patients with LV hypertrophy and non-Q-wave AMI have smaller enzymatic infarcts and the same short-term prognosis as do patients without LV hypertrophy, their reinfarction and mortality rates are significantly increased during the first year of follow-up.(ABSTRACT TRUNCATED AT 250 WORDS)     

Angiographic findings after myocardial infarction in patients with previous bypass surgery: explanations for smaller infarcts in this group compared with control patients

The incidence of previous coronary artery bypass surgery (CABS) in patients with acute myocardial infarction admitted to our hospital has risen from 2.3% to 11.2% in 6 years. We compared infarct size and the angiographically determined cause of infarction in 52 control patients and in 52 consecutive patients with acute myocardial infarction at least 2 months after they had undergone CABS. Baseline characteristics were similar in both groups except for a higher incidence of preexisting Q waves in the post-CABS group (22 vs 10; p less than .05). Indexes of myocardial infarct size were smaller in the post-CABS group compared with those in control patients: peak creatine kinease (CK) level (IU/liter) 1113 +/- 1094 (mean +/- SD) vs 1824 +/- 1932 (p less than .01), peak CK-MB level (IU/liter) 173 +/- 230 vs 272 +/- 332 (p less than .02), peak summed ST segment elevation (mm) 3.5 +/- 4.8 vs 8.2 +/- 9.9 (p less than .005), and QRS score on days 7 to 10, 1.9 +/- 3.0 vs 4.3 +/- 3.4 (p less than .001). Postinfarction left ventricular ejection fraction was higher in the post-CABS group (53 +/- 13%) compared with that in control patients (47 +/- 12%; p less than .05). The incidence of total occlusion of the artery to the infarct zone was similar in the post-CABS and control patients (33 vs 27), as was the incidence of one-, two-, and three-vessel disease (artery plus graft). Collateral blood flow to the infarct zone was found in 27 post-CABS patients and in 23 control patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of angina pectoris before first acute myocardial infarction

To delineate the clinical significance and prognostic importance of a history of chronic or new onset angina pectoris before acute myocardial infarction (AMI), 732 consecutive patients admitted for a first AMI were studied and divided into 3 groups. Two hundred patients (27%) had chronic angina before AMI (greater than 1 month); 247 patients (34%) had new onset angina before AMI (less than 1 month) and the 285 remaining patients (39%) never had angina before AMI. All clinical characteristics were similar in the group of patients with chronic angina and in the group of patients with new onset angina, including in-hospital mortality (10 vs 9%) and 3-year post-hospital mortality (16 vs 16%). Compared to the 285 patients without angina, the 447 patients with angina before AMI were older, more likely to be women, and had a higher frequency of anterior AMI and early post-infarction angina. Both groups had a similar in-hospital mortality (10 vs 8%, not significant), but patients with angina had a higher 3-year post-hospital mortality (16 vs 7%, p less than 0.001). In the group of patients with angina before AMI who were discharged from the hospital, the comparison of nonsurvivors and survivors showed that the patients who died were older, presented more frequently with a non-Q-wave myocardial infarct and more often had left ventricular failure and complete bundle branch block during hospital stay. Chronic and new onset angina before AMI have the same clinical characteristics and deleterious long-term prognostic significance.     

Significance of Q-wave regression after transmural acute myocardial infarction

A total of 313 consecutive patients was studied to assess the prevalence and prognostic implications of Q-wave loss after transmural acute myocardial infarction. Heart catheterization, including single-plane left ventriculography and selective coronary arteriography, was performed before hospital discharge. After a mean follow-up of 65 (1 to 100) months, 34 patients (11%) lost their Q waves. The time interval from the acute event to the first electrocardiogram showing Q-wave disappearance was 14 (1 to 32) months. Peak creatine kinase value was significantly higher in patients who retained their Q waves than in those who lost them (1,121 +/- 813 vs 779 +/- 464 IU, respectively, p less than 0.05). Severity of coronary artery disease, as judged by the number of diseased arteries and the number of arteries with total or subtotal occlusion, was similar in both groups. However, patients showing Q-wave regression had lower left ventricular end-diastolic pressure, higher ejection fraction and fewer abnormally contracting segments than their counterparts (12 +/- 6 vs 15 +/- 7 mm Hg, p less than 0.05; 53 +/- 11 vs 44 +/- 14%, p less than 0.001; 1 +/- 1 vs 2 +/- 1 segments, p less than 0.001, respectively). In addition, no patient with normalized electrocardiogram presented with left ventricular aneurysm. Although differences in mortality, nonfatal reinfarction and new onset of angina between the 2 groups were not significant, congestive heart failure was prevalent among patients with permanent Q waves (23 vs 6%, p less than 0.05). Our findings suggest that Q-wave loss after AMI may be related to a smaller infarct size.     

Diabetes mellitus prevents ischemic preconditioning in patients with a first acute anterior wall myocardial infarction

OBJECTIVES: This study was undertaken to assess whether prodromal angina could have beneficial effects in diabetic patients with acute myocardial infarction (AMI). BACKGROUND: Prodromal angina occurring shortly before the onset of AMI is associated with favorable outcomes by the mechanism of ischemic preconditioning. However, little is known about the impact of diabetes on ischemic preconditioning. METHODS: We studied 611 patients with a first anterior wall AMI who underwent emergency catheterization within 12 h after the onset of chest pain: 490 patients without diabetes and 121 patients with non-insulin treated diabetes. Prodromal angina was defined as angina episode(s) occurring within 24 h before the onset of AMI. Serial contrast left ventriculograms were obtained in 424 patients at the time of acute and predischarge catheterization. RESULTS: In non-diabetic patients, prodromal angina was associated with lower peak creatine kinase (CK) value (3,068 +/- 2,647 IU/l vs. 3,601 +/- 2,462 IU/l, p = 0.037), larger increase in left ventricular ejection fraction (LVEF) (10.1 +/- 13.0% vs. 5.8 +/- 13.4%, p = 0.004) and lower in-hospital mortality (3.4% vs. 9.3%, p = 0.015). On the contrary, in diabetic patients, there was no significant difference in peak CK value (3,382 +/- 2,520 IU/l vs. 3,233 +/- 2,412 IU/l, p = NS), the change in LVEF (6.7 +/- 13.8% vs. 7.1 +/- 12.4%, p = NS) and in-hospital mortality (8.8% vs. 11.0%, p = NS) between patients with and patients without prodromal angina. CONCLUSIONS: Prodromal angina limited infarct size, enhanced recovery of LV function and improved survival in non-diabetic patients with AMI. However, such beneficial effects of prodromal angina were not observed in diabetic patients, suggesting that diabetes might prevent ischemic preconditioning.     

Prognosis in acute myocardial infarction in relation to development of Q waves.

In a totally nonselected group of patients with acute myocardial infarction (AMI) (n = 921) admitted from the emergency department to the coronary care unit or other hospital ward, the occurrence of non-Q-wave AMI and the prognosis in these patients was determined and compared with those in whom Q waves were developed. Fifty-two percent had AMI without new Q waves. Patients with a non-Q-wave AMI differed from patients with Q-wave AMI, more frequently having a previous history of AMI (p less than 0.001), angina pectoris (p less than 0.01), diabetes mellitus (p less than 0.05), congestive heart failure (p less than 0.001), and a higher mean age (p less than 0.001), whereas smoking was more common in Q-wave AMI. Patients with non-Q-wave AMI had a 1-year mortality of 31% compared with 26% in Q-wave AMI (p greater than 0.2) and a reinfarction rate of 20% compared with 12% for Q-wave AMI (p less than 0.01). Among patients aged less than 75 years without a previous history of AMI, congestive heart failure, and diabetes mellitus, the 1-year mortality rate was 16% for patients with Q waves versus 15% for those without Q waves (NS). Appearance of Q waves was not independently associated with death. We conclude that in a nonselected group of patients with AMI the occurrence of a non-Q-wave AMI is much higher than previously reported. The prognosis in AMI during one year of follow-up is not associated with development of Q waves.     

Long-term prognosis after first Q-wave (transmural) or non-Q-wave (nontransmural) myocardial infarction: analysis of 593 patients

Follow-up results in 593 patients less than or equal to 7 years (mean 4.7) after hospital discharge for their first myocardial infarction (MI) are presented. Patients were grouped according to the presence or absence of Q waves on electrocardiograms after the MI and by peak serum glutamic oxalacetic transaminase (SGOT) level during hospitalization. Cardiac mortality varied. Patients with Q-wave infarcts and an SGOT level less than or equal to 240 IU/liter had a cardiac mortality of 3.1% per year, whereas patients with Q-wave MI and an SGOT level greater than 240 IU/liter had an 11% 6-month mortality and a 3.8% per year cardiac mortality thereafter. However, patients with non-Q-wave (nontransmural) MI had a excellent survival rate for 2 years (96.8%) which continued in patients aged less than or equal to 60 years thereafter. However, patients with non-Q-wave infarcts aged greater than 60 years had a 12% per year cardiac mortality in the third post-MI year and an additional 12% died each year thereafter. Early mortality was related to enzyme level, whereas late mortality was a function of type (Q-wave or non-Q-wave) and age.     

Diagnostic and prognostic implications of transient isolated negative T waves in suspected acute myocardial infarction

The diagnostic and prognostic implications of transient isolated negative T waves were studied in 127 patients in whom acute myocardial infarction (AMI) was suspected. Eight-four patients with no AMI and no electrocardiographic changes served as the control group. The 2 groups were well matched. Twenty-nine patients (23%) with isolated negative T wave had a significant increase in serum creatine kinase (CK)-MB levels and fulfilled the diagnostic criteria for AMI. The increase in serum CK-MB levels did not predict a higher risk of hospital mortality, but during follow-up (median 31 months), a serum CK-MB level above 30 U/liter identified patients with a significantly increased risk of dying (p less than 0.05). Both the number of affected electrocardiographic leads and the sum of negative T-wave amplitudes were significantly related to the follow-up mortality rate (p less than 0.01). The comparison between control subjects and patients with negative T waves during follow-up showed more events among the patients: AMI (17% vs 8%, p less than 0.02); death (24% vs 12%, p less than 0.01); and AMI or death (31% vs 19%, p less than 0.01). Thus, only 25% of patients with aggravated chest pain and isolated negative T waves have AMI. However, the long-term prognosis for the entire group of patients with isolated negative T waves is poor, and any therapeutic intervention should be initiated immediately.     

Acute myocardial infarct in persons over 70. The results and differential characteristics

Distinctive features of patients over 70 years with acute myocardial infarction (AMI) are studied. Between May 1988 and April 1989, 420 patients with AMI were admitted to our hospital; 118 of them (28.5%) were older than 70 years. In this group of patients, proportion of woman was higher (36 vs 16%, p less than 0.001), while incidence of smoking and hypercholesterolemia was lower (41 vs 64%, p less than 0.001; and 15 vs 29%, p less than 0.05). There was no differences in other risk factors, prior history of coronary heart disease (angina, AMI, coronary surgery), or general features of AMI (location, proportion of painless AMI, non-Q-wave AMI, evolved AMI, initial admission to coronary care unit or general ward, time from the beginning of symptoms to admission, residual ejection fraction). The incidence of severe complications was superior between older patients: shock, 17 vs 7% (p less than 0.05); Killip class III/IV, 30 vs 13% (p less than 0.001); and fascicular blocks: 26 vs 16% (p less than 0.05). Hospital mortality was also higher in older patients, 25.5 vs 14% (p less than 0.01). No patients older than 70 years received fibrinolytic therapy, and only one underwent coronary artery surgery (22% and 15%, respectively, in younger patients). Coronary arteriography, exercise test, radionuclide ventriculography and Holter monitoring were also performed before discharge in a lesser proportion in older patients. We conclude that mortality and severe complications were higher between patients over 70 years with AMI. We think that mortality could be decreased by a more aggressive management in, at least, selected groups of older patients with AMI.     

Prognostic significance and beneficial effect of diltiazem on the incidence of early recurrent ischemia after non-Q-wave myocardial infarction: results from the Multicenter Diltiazem Reinfarction Study

Of 576 patients with non-Q-wave acute myocardial infarction enrolled in the Diltiazem Reinfarction Study, 246 (43%) had 1 or more episodes of angina at rest or with minimal effort during 10.5 days of treatment with either diltiazem (90 mg every 6 hours) or placebo. Reinfarction (12.2% vs 3.6%, p less than 0.0001) or death (6.1% vs 1.5%, p = 0.003) was more likely to occur within 2 weeks of randomization in patients with postinfarction angina than in those without angina. Based on serial electrocardiographic data, 115 of the 246 patients with angina had transient ST-T changes and 131 did not. Comparison of the 14-day event rates in these 2 groups showed that the 115 patients with electrocardiographic evidence of ischemia had a higher frequency of reinfarction (20% vs 5.3%, p less than 0.001), more extensive damage as assessed by peak MB-creatine kinase levels (91 +/- 76 vs 37 +/- 19 IU/liter, p = 0.059 [Wilcoxon rank sum]) and a higher mortality rate (11.3% vs 1.5%, p = 0.001). Angina associated with transient ST-T changes occurred in 70 of the 289 patients in the placebo group but in only 45 of the 287 patients in the diltiazem group--a 28% reduction in cumulative life-table incidence (p = 0.0103 [2-tail, log rank]; 95% confidence interval, 9.3 to 53.8%). It is concluded that patients with early postinfarction angina are at increased risk of reinfarction and death, and angina associated with transient electrocardiographic changes identified a very high risk subset. This subset appeared to have a larger area of viable but jeopardized myocardium and benefited from prophylactic therapy with diltiazem.     

Early use of beta-blockers is associated with attenuation of serum C-reactive protein elevation and favorable short-term prognosis after acute myocardial infarction

BACKGROUND: We have reported that a marked elevation in serum C-reactive protein (CRP) level is a predictor for infarct expansion and cardiac rupture after AMI. Although beta-blockers prevent cardiac rupture after AMI, their effect on serum CRP elevation has not been determined. METHODS: We studied a total of 154 patients with first Q-wave AMI. Patients complicated by pump failure were excluded from this study. Eighty-two patients received beta-blocker treatment within 24 h of the onset of AMI, while 72 patients received no beta-blocker treatment. Peak serum creatine kinase (CK) and CRP levels were determined by serial measurements. RESULTS: There was no difference between the groups according to age, sex, coronary risk factors, pre-infarction angina, infarct site, prior use of cardiovascular drugs, use of revascularization therapy, and prevalence of multivessel disease. Beta-blocker treatment was associated with a lower peak CRP level (6.9 +/- 6.1 vs.10.8 +/- 9.3 mg/dl, p = 0.002), a shorter duration from the onset to the peak CRP level (2 +/- 1 vs. 3 +/- 2 days, p < 0.0001), a lower incidence of cardiac rupture (p = 0.03) and lower in-hospital cardiac mortality (p = 0.02), despite similar peak CK levels. CONCLUSION: The early use of beta-blockers is associated with decreased serum CRP level and a favorable clinical outcome after first Q-wave AMI, suggesting some beneficial effects of beta-blockers on infarct healing after AMI.     

C-reactive protein in patients with acute coronary syndrome: correlation with diagnosis, myocardial damage, ejection fraction and angiographic findings

BACKGROUND: C-reactive protein (CRP) plasmatic levels increase in patients with acute coronary syndromes (ACS). Correlations between CRP levels, myocardial functional damage and cardiomyocyte lysis remain to be defined. METHODS: 192 consecutive patients with acute coronary syndromes (64.97 +/- 11.08 mean age, 71.35% male gender) were included in the study; 138 patients (71.87%) were discharged with an acute myocardial infarction (AMI) diagnosis (28 with non Q-wave AMI) and 54 with an unstable angina (UA) diagnosis (28.13%). In all patients CRP, CK, LDH, CK-MB and troponin I plasmatic concentrations were evaluated every 6 h for 48 h and every 24 h for the following 2 days from the onset of symptoms. Ejection fraction was estimated by bidimensional echocardiography and extension of myocardial lysis by cardiac enzymes plasmatic release. 92 patients (67 with AMI, 25 with UA) underwent coronary-angiography. Incidence of adverse cardiac events was recorded in a 6 months follow up. RESULTS: Mean CRP levels in Q-wave MI showed a statistically significant increase in the different blood samples with baseline. Mean CRP levels of the three groups were not statistically different at baseline and after 6, 12, and 18 h. Q-wave AMI CRP levels showed a statistically significant difference as against non Q-wave AMI at 36 (p < 0.05), 48 (p < 0.05) and 72 h (p < 0.05) and UA at 24 (p < 0.01), 30 (p < 0.01), 48 (p < 0.0001), 72 (p = 0.0001) and 96 h (p = 0.0003); non Q-wave AMI CPR levels showed a statistically significant difference as against UA at 48 h (p < 0.01). CRP peak mean levels were significantly different when comparing Q-wave AMI patients with UA patients (8.21 +/- 7.85 vs. 2.75 +/- 3.33 mg/dl, p < 0.001). In patients with Q-wave AMI there was a correlation between CRP peak concentrations and CK (r = 0.264, p = 0.008) and LDH (r = 0.32, p = 0.001), while correlation with CK-MB peak concentrations was not statistically significant (r = 0.196, p = 0.051). In the same patient group, there was also a correlation between CRP plasmatic concentrations and troponin I plasmatic concentrations from the 30th to 96th h after the onset of symptoms (r = 0.38-0.53, p < 0.05). No correlation was found between CRP levels and ejection fraction and angio-coronarography findings (number of stenotic vessels, culprit lesions, ruptured plaques). Peak CRP levels were associated in a 6 months follow up with an increased incidence of major adverse cardiac events (MACEs) in patients with Q-wave AMI (HR 1.1649, 95% C.I. 1.0197-1.3307, p < 0.05). CONCLUSIONS: CRP plasmatic concentrations showed a different release curve in patients with Q-wave AMI in comparison with patients with non Q-wave AMI and with patients with UA. CRP peak concentrations did not correlate with ejection fraction and angiographic findings, but correlate with incidence of MACE. The increase in CRP levels during Q-wave MI seems to be linked to the extension of myocardial damage rather than pre-existing inflammation.     

Relation of peak creatine kinase levels during acute myocardial infarction to presence or absence of previous manifestations of myocardial ischemia (angina pectoris or healed myocardial infarction)

The hypothesis that acute myocardial infarction (MI) is more extensive in patients without previous angina or healed MI was evaluated in 177 patients with documented recent acute MI. Ninety-nine patients (56%) had no previous angina or healed MI (negative history group), and the remaining 78 patients (44%) had a previous history of angina or healed MI (positive history group). The mean peak creatine kinase (CK) level in the negative history group was 784 compared with 419 IU in the positive history group (p less than 0.0001). The mean peak CK-MB level in the negative history group was 128 compared with 76 IU in the positive history group (p less than 0.001). The mean peak CK-MB level was higher in the negative history group after controlling for age, streptokinase administration, previous coronary artery bypass grafting or treatment with beta-blocking agents. Despite the high frequency of healed MI in the positive history group (73%), the rates of in-hospital complications were similar for the 2 groups. Patients with acute MI without previous angina or healed MI have substantially higher peak CK and CK-MB levels; this implies a larger MI than in patients with previous angina or healed MI.     

Long-term prognosis after myocardial infarction in patients with previous coronary artery bypass surgery

A group of 205 patients hospitalized with myocardial infarction 2 to 162 months (mean 66) after bypass surgery and 205 control patients with myocardial infarction were compared and followed up for 34 +/- 25 months after hospital discharge. At baseline the postbypass group contained more men (p less than 0.03) and more patients with previous myocardial infarction (p less than 0.06), but the groups were otherwise comparable. Indexes of infarct size were lower in postbypass patients: sum of ST elevation, QRS score, peak serum creatine kinase (CK) (1,115 +/- 994 versus 1,780 +/- 1,647 IU/liter) and peak MB CK (all p less than or equal to 0.001). Postmyocardial infarction ejection fraction was 45 +/- 15% in the postbypass group and 43 +/- 15% in the control group (p = NS); in-hospital mortality rate was 4 and 5%, respectively (p = NS). When patent grafts were taken into account, the two groups were comparable in extent of coronary artery disease. At 5 years after discharge, cumulative mortality was similar in the postbypass and control groups (30 versus 25%, respectively, p = NS). However, postbypass patients had more reinfarctions (40 versus 23%, p = 0.007), more admissions for unstable angina (23 versus 18%, p = 0.04) and more revascularization procedures (34 versus 20%, p = 0.04) than did control patients. The total for these events at 5 years was 70% in the postbypass group and 49% in the control group (p = 0.001). Thus, although patients with previous bypass surgery who develop acute myocardial infarction have a smaller infarct, their subsequent survival is no better than that of other patients with acute myocardial infarction. They experience more reinfarctions and unstable angina. Previous bypass surgery is an important clinical marker for recurrent cardiac events after myocardial infarction.     

Factors leading to shorter survival after acute myocardial infarction in patients ages 65 to 75 years compared with younger patients

Although the number of elderly patients with acute myocardial infarction (AMI) has steadily increased and these patients are known to have a higher early subsequent mortality than younger patients, the reasons for this adverse prognosis are poorly understood. We compared the clinical courses of 217 patients, ages 65 to 75 years, with 631 patients younger than 65 years of age enrolled in the Multicenter Investigation of the Limitation of Infarct Size (MILIS). The older group had a higher prevalence of adverse baseline risk factors, including history of congestive heart failure (14 vs 7%, p less than 0.001), previous AMI (28 vs 22%, p less than 0.05), angina pectoris (42 vs 34%, p less than 0.05), systemic hypertension (64 vs 52%, p less than 0.01), diabetes mellitus (24 vs 17%, p less than 0.05) and female gender (37 vs 24%, p less than 0.001). Despite having a smaller infarct size index than younger patients (15 +/- 1 vs 18 +/- 1 CK-MB g-Eq/m2, p less than 0.002), the elderly patients had a lower admission left ventricular ejection fraction (43 +/- 1 vs 47 +/- 1%, p less than 0.01) and a higher frequency of clinical congestive heart failure (44 vs 28%, p less than 0.001) and in-hospital death (14 vs 7%, p less than 0.01). The 1-year mortality for elderly hospital survivors was also markedly greater (19 vs 5%, p less than 0.001) as was the 4-year mortality (35 vs 13%, p less than 0.001). Adjustment for 7 adverse baseline characteristics in the elderly could account for their increased in-hospital mortality. However, these and 12 additional in-hospital characteristics did not account for the increased 1- and 4-year mortalities of the elderly hospital survivors, which are presumably affected by variables not included in the present age-associated study.     

急性心肌梗死再灌注心律失常不增加心肌损伤

目的探讨急性心肌梗死（AMI）患者PCI再灌注心律失常的临床意义。方法回顾性分析近年在我院接受直接PCI且成功开通梗死相关血管（IRA）的AMI患者228例。将其中开通IRA后数分钟内发生心肌缺血再灌注损伤（MIRI）的119例患者（MIRI组）分为3个亚组,即严重心动过缓和低血压（缓慢性心律失常组）、需电复律的严重室性心律失常（快速性心律失常组）和IRA前向血流≤TIMI2级且除外急性闭塞（无复流组）。结果（1）临床和造影资料：与无MIRI组相比,MIRI组缺血时间短,梗死前心绞痛所占比例低,多支血管病变、下壁梗死、右冠状动脉IRA、PCI前IRA血流TIM10级和肾功能不全所占比例高,住院病死率较高（13．4％比4．6％,P=0．021）。（2）血清心肌酶水平：缓慢性心律失常组肌酸激酶（OK）峰值中位数显著低于无MIRI组（20LOIU／L比2521IU／L,P=0．039）,肌酸激酶同工酶（CK．MB）峰值中位数有低于无MIRI组的趋势（98IU／L比142IU／L,P=0．091）;快速性心律失常组CK峰值中位数（2317IU／L）和CK-MB峰值中位数（134IU／L）与无MIRI组相比差异无统计学意义（P=0．627,0．500）;无复流组CK峰值中位数（4573IU／L）和CK-MB峰值中位数（338IU／L）均显著高于无MIRI组（P均=0．000）。（3）超声心功能：无复流组左心室射血分数显著低于无MIRI组（38．7％±8．3％比51．2％±8．1％,P=0．000）,左心室舒张末期容积显著大于快速性心律失常组[（135±32）ml比（105±19）ml,P=0．029],左心室收缩末期容积显著大于无MIRI组[（82±33）ml比（54±24）ml,P=0．008]和缓慢性心律失常组[（56±19）ml,P=0．025]。结论再灌注心律失常可能提示梗死区存活心肌多,而且不增加心肌损伤;无复流增加心肌损伤,导致永久的心功能障碍。