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)     

Electrocardiographic evolution of posterior acute myocardial infarction: importance of early precordial ST-segment depression

Precordial ST-segment depression is typically observed in anterior non-Q-wave acute myocardial infarction (AMI), and is generally not regarded as an indication for acute thrombolytic therapy. Of 544 patients with creatine kinase (CK)-MB-confirmed non-Q-wave AMI randomized to the prospective multicenter Diltiazem Reinfarction Study, 50 patients (9.2%) had isolated precordial ST-segment depression of 1 mm or more in 2 or more contiguous precordial electrocardiographic leads (V1-V4). Serial electrocardiograms recorded at study entry (mean 50.5 hours after onset of chest pain), on study day 2, study day 3 and at predischarge showed that in 23 of 50 patients (40%) electrocardiographic evidence of posterior AMI evolved, defined as an R wave of 0.04 second or more in lead V1 and an R:S greater than or equal to 1 in lead V2. In 18 of these 23 patients (78%), posterior AMI had evolved by study day 3, and none had an abnormal reelevation of CK-MB (every 12-hour sampling) for up to 14 days of hospitalization. Compared with the remaining 27 patients who had electrocardiographic features of anterior non-Q-wave AMI only, the 23 with initial precordial ST segment depression in whom posterior AMI developed had significantly higher mean peak CK values (1,051 +/- 172 vs 663 +/- 89 IU, p less than 0.009) and greater mean precordial ST-segment depression in lead V1 (0.28 vs + 0.19 mm, p = 0.01), in lead V2 (1.3 vs 0.26 mm, p = 0.003) and in lead V3 (2.0 vs 0.93 mm, p = 0.0004).(ABSTRACT TRUNCATED AT 250 WORDS)     

Prognostic significance of a low peak serum creatine kinase level in acute myocardial infarction

To assess the prognostic significance of a low peak creatine kinase (CK) level, 723 consecutive patients admitted with acute myocardial infarction (AMI) within 16 hours after onset of symptoms were studied. Thrombolytic therapy was not attempted during the study. Patients were dichotomized according to their peak CK levels, determined from a cluster analysis of peak CK distribution among the population of patients who died within 3 years after hospital discharge. The 139 patients with low peak CK (less than or equal to 650 IU/liter) (group 1) were compared to the 584 patients with high peak CK (greater than 650 IU/liter) (group 2). Patients in group 1 were older and had a higher incidence of previous AMI, angina pectoris before AMI and non-Q-wave AMI. Despite a lower incidence of in-hospital complications and a nonsignificantly lower hospital mortality rate (4 vs 9%) the group 1 three-year posthospital mortality rate was higher (26 vs 17%; p less than 0.02), especially in the subgroup of patients with a Q-wave infarct (mortality 31% in group 1 vs 16% in group 2; p less than 0.001). Among the 491 patients who had a first Q-wave AMI, 55 had a peak CK less than or equal to 650 IU/liter. Compared to the 436 patients with a higher peak CK, these 55 patients had a higher incidence of early postinfarction angina (31 vs 14%; p less than 0.01), a similar hospital mortality (4 vs 7%) but a higher 3-year posthospital mortality (23 vs 12%; p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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)     

Non-Q- and Q-wave infarction after thrombolytic therapy with intravenous streptokinase for chest pain and anterior ST-segment elevation

The clinical features of patients treated with streptokinase for chest pain and anterior ST-segment elevation who subsequently develop non-Q-wave infarction are unknown. Of the 75 consecutive patients who initially presented with chest pain and ST-segment elevation in the anterior leads (V1-V6, I, aVL) and were treated with intravenous streptokinase (time from symptoms to treatment averaged less than 3 hours), 32 (43%) developed a non-Q-wave and 43 (57%) a Q-wave myocardial infarction. Twenty seven of 32 patients (84%) from the non-Q-wave group and 39 of 43 (91%) from the Q-wave group were studied by angiography at 5.16 +/- 2.88 days after the onset of myocardial infarction. Left ventricular end-diastolic pressure was 13 +/- 6 vs 20 +/- 7 mm Hg (p less than 0.001), left ventricular ejection fraction was 60 +/- 8 vs 49 +/- 14% (p less than 0.001) and the infarct vessel patency rate was 85 vs 72% (p = 0.44) in patients with a non-Q versus a Q-wave infarction, respectively. In summary, when patients presenting with chest pain and ST-segment elevation are treated with streptokinase, a significant portion of these symptoms will evolve into a non-Q-wave infarction. Patients with a non-Q-wave infarction will have a better preserved left ventricular function than patients who develop a Q-wave infarction. This suggests the need for equal distribution of such patients in randomized trials of thrombolytic therapy for acute myocardial infarction to avoid misinterpreting data between groups.     

Differential long-term impact of in-hospital symptoms of psychological stress after non-Q-wave and Q-wave acute myocardial infarction.

Because of their unstable pathophysiology, it was hypothesized that patients with non-Q-wave acute myocardial infarctions (AMI) would be more vulnerable to the negative effects of psychological stress than patients with Q-wave AMI, and thus would be more likely to benefit from programs aimed at relieving stress. This hypothesis was tested through secondary analysis of data from a 1-year randomized clinical trial of psychological stress monitoring and intervention after AMI. After discharge, treatment group patients were telephoned each month and asked to respond to an index of psychological stress symptoms (General Health Questionnaire GHQ-20). Those with high stress symptoms (GHQ greater than or equal to 5) received home nursing visits. Control group patients received usual care. The sample consisted of 461 men, aged 31 to 86 years, who responded to the GHQ-20 before hospital discharge. Patients were followed for 5 years using record data. There were 321 Q-wave AMIs, 112 non-Q-wave AMIs and 28 indeterminate electrocardiograms. Life-table analyses showed that among patients with non-Q-wave AMIs receiving usual care, high stress in the hospital (GHQ greater than or equal to 5) was associated with a 1-year relative risk (RR) of cardiac mortality of 5.49 +/- 1.39 (p = 0.01). In comparison, control patients with Q-wave MIs had no stress-related increase in risk (RR = 0.41 +/- 2.08, p = 0.40). In the treatment group, the patients with non-Q-wave AMIs did not experience an increase in risk associated with high stress (RR = 1.80 +/- 1.79, p = 0.52).(ABSTRACT TRUNCATED AT 250 WORDS)     

Q-wave evolution of a first acute myocardial infarction without significant ST segment elevation

BACKGROUND: Some patients with acute myocardial infarction presenting without significant ST segment elevation develop a Q-wave infarction. It is unclear whether these patients can be identified from the admission electrocardiogram (ECG) and whether they differ in their in-hospital prognosis from those who retain a non-Q-wave myocardial infarction. METHODS: In 432 consecutive patients admitted to our centre with a first acute myocardial infarction without Q waves and with ST segment amplitudes < or =0.1 mV on admission, we assessed the frequency, the electrocardiographic predictors and the short-term implications of a Q-wave evolution. RESULTS: In 94 patients (22%), a Q-wave myocardial infarction evolved before hospital discharge (14 anterior, 26 inferior, six lateral, and 48 posterior). Minor anterior ST segment elevation was 36% sensitive and 95% specific in predicting anterior Q waves; minor inferior ST segment elevation, 42% and 89%, respectively, for inferior Q waves; and a maximal ST segment depression > or =0.2 mV in leads V2-V3 with upright T waves and without remote ST segment depression, 38% and 97%, respectively, for posterior R waves. Although patients with a Q-wave evolution had a greater creatinkinase MB peak than those retaining a non-Q-wave pattern (191+/-113 vs. 105+/-77 IU/l, respectively, P<0.001), they experienced a benign in-hospital course, with similar risk of severe complications after adjustment for the baseline clinical predictors than non-Q-wave patients. CONCLUSIONS: About one fifth of patients with a first acute myocardial infarction without a significant ST segment elevation develop a Q-wave infarction and the admission ECG can help identify them. This evolution, however, is not associated with a worse in-hospital outcome.     

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.     

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.     

Immediate and long-term results of delayed recanalization of occluded acute myocardial infarction-related arteries using coronary angioplasty.

Recent evidence suggests that late reperfusion of an occluded infarct-related artery after acute myocardial infarction (AMI) may convey a better prognosis. The clinical outcome of percutaneous transluminal coronary angioplasty (PTCA) as a means of mechanical reperfusion in this particular setting has not been clearly delineated. Ninety-seven patients with AMI underwent PTCA of the occluded infarct-related artery after the acute phase of the AMI (48 hours to 2 weeks, mean 8 +/- 4 days). The study consisted of 72 men (74%) (mean age 56.5 +/- 12 years) and 25 women. Seventy-seven patients (79%) had a Q-wave AMI and 20 patients (21%) a non-Q-wave AMI. Seventy-six patients (79%) had angina after AMI and 4 had previously undergone coronary bypass surgery. Clinical success was achieved in 85 patients (87%). Angiographic success was obtained in 90 of the 97 occluded arteries (93%) and was similar for all 3 major vessels: right coronary 97%, left anterior descending 93% and circumflex 85% (p = not significant). Major complications (AMI, emergency bypass and death) occurred in 3 patients (3.1%). Long-term follow up (3.7 +/- 0.8 years) revealed symptomatic recurrence in 20 (23%), whereas 51 (58%) remained asymptomatic. Most recurrences (16 of 20) were in the form of restenosis rather than reocclusion, with a high success rate for repeat dilation (93%). These results indicate that mechanical reperfusion of an occluded infarct artery, performing PTCA 48 hours to 2 weeks after AMI, has a high success rate, a low complication rate and low symptomatic restenosis.     

Association of patency of the infarct-related coronary artery with plasma levels of plasminogen activator inhibitor activity in acute myocardial infarction.

To examine the fibrinolytic capacity in patients with acute myocardial infarction (AMI), baseline levels of plasma plasminogen activator inhibitor (PAI) activity and tissue-type plasminogen activator (t-PA) antigen were measured in 47 patients with Q-wave AMI who underwent emergent coronary angiography 3.0 +/- 0.2 hours after the symptom onset. They received intracoronary injection of urokinase if their infarct-related arteries were occluded. They were classified into 3 groups according to the patency of the infarct-related artery before and after thrombolytic therapy: the patent group (13 patients), the recanalized group (23 patients) and the occluded group (11 patients). The mean level of plasma PAI activity (IU/ml) was higher in patients with AMI as a whole than in the control group (12.8 +/- 1.6 vs 5.4 +/- 0.5, p less than 0.01). The level was lower in the patent group (3.0 +/- 1.1) and higher in the recanalized (18.6 +/- 2.2) and occluded (10.8 +/- 2.5) groups than in the control group (each p less than 0.01). The level was lower in the occluded than in the recanalized group (p less than 0.01) and 62% of the patients in the occluded group had levels within range of the control group. The mean level of plasma t-PA antigen (ng/ml) was higher in patients with AMI as a whole than in the control group (10.3 +/- 0.8 vs 5.8 +/- 0.3, p less than 0.01). There was no difference in the level among the 3 groups with AMI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Electrocardiographic subset analysis of diltiazem administration on long-term outcome after acute myocardial infarction. The Multicenter Diltiazem Post-Infarction Trial Research Group

The effect of diltiazem on long-term outcome after acute myocardial infarction (AMI) was assessed in 2,377 patients enrolled in the Multicenter Diltiazem Post-Infarction Trial and subsequently followed for 25 +/- 8 months. The study population included 855 patients (36%) with at least 1 prior AMI before the index infarction and 1,522 patients (64%) with a first AMI, of whom 409 (27%) had a first non-Q-wave AMI, 664 (44%) a first inferior Q-wave AMI, and 449 (30%) a first anterior Q-wave AMI. This post hoc analysis revealed that, among patients with first non-Q-wave and first inferior Q-wave AMI, there were fewer cardiac events during follow-up in the diltiazem than in the placebo group, and that the reverse was true for patients with first anterior Q-wave AMI or prior infarction. The diltiazem:placebo Cox hazard ratio (95% confidence limits) for the trial primary end point (cardiac death or nonfatal reinfarction, whichever occurred first) was: first non-Q-wave AMI-0.48 (0.26, 0.89); first inferior Q-wave AMI-0.66 (0.40, 1.09); first anterior Q-wave AMI-0.82 (0.51, 1.31); and prior AMI-1.11 (0.85, 1.44). Use of cardiac death alone as an end point gave an even more sharply focused treatment difference: first non-Q-wave AMI-0.46 (0.18, 1.21); first inferior Q-wave AMI-0.53 (0.27, 1.06); first anterior Q-wave AMI-1.28 (0.68, 2.40); prior infarction-1.26 (0.90, 1.77). Further analysis revealed that these differences in the effect of diltiazem in large part reflected the different status of the 4 electrocardiographically defined subsets in terms of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)     

Troponin T elevation after successful directional atherectomy

BACKGROUND: The incidence and correlates of postinterventional cardiac troponin T (cTnT) elevation have not been evaluated in patients with successful directional atherectomy (DCA). METHODS: Total creatine kinase (CK) activity, CK-MB mass concentrations and cTnT levels were measured in 36 patients before, and serially 4, 24, 48 and 72 hours after successful DCA. Patients were followed for death, Q-wave infarction, need for emergency bypass surgery, periprocedural vascular complications (transient in-lab vessel closure, side branch compromise, large dissection), and non-Q-wave infarction on ECG. Patients were followed for clinical outcomes and angiographic restenosis for 6 months. Vascular correlates were studied by coronary angiography and intravascular ultrasound before, immediately after and 4 hours after elective and successful DCA. RESULTS: 25 patients (69.4%) had elevated levels of cTnT, whereas CK-MB mass > or = 6 ng/ml and mild elevations of total CK activity were present in only 36.1 and 5.6%, respectively. Elevated cTnT was related to vascular complications in 44% of cases. Inapparent microembolization of platelets or plaque debris was considered responsible for most of the remaining micronecroses. During 6 month follow-up rates of clinical restenosis (44 vs 9%, p = 0.059) tended to be higher in patients with as compared to patients without cTnT release after DCA. CONCLUSION: Successful DCA is associated with postprocedural elevations of cTnT which relate to minor vascular complications and presumably microembolization of platelets or plaque debris. The superior diagnostic performance of cTnT compared to CK-MB mass may relate to more sensitive identification of microinfarction. Further studies are mandatory to confirm the association between elevation of cTnT and risk of restenosis and TVR.     

Troponin T elevation after successful directional atherectomy

Background The incidence and correlates of postinterventional cardiac troponin T (cTnT) elevation have not been evaluated in patients with successful directional atherectomy (DCA). Methods Total creatine kinase (CK) activity, CK-MB mass concentrations and cTnT levels were measured in 36 patients before, and serially 4, 24, 48 and 72hours after successful DCA. Patients were followed for death, Q-wave infarction, need for emergency bypass surgery, periprocedural vascular complications (transient in-lab vessel closure, side branch compromise, large dissection), and non-Q-wave infarction on ECG. Patients were followed for clinical outcomes and angiographic restenosis for 6months. Vascular correlates were studied by coronary angiography and intravascular ultrasound before, immediately after and 4hours after elective and successful DCA. Results 25 patients (69.4%) had elevated levels of cTnT, whereas CK-MB mass ≥6ng/ml and mild elevations of total CK activity were present in only 36.1 and 5.6%, respectively. Elevated cTnT was related to vascular complications in 44% of cases. Inapparent microembolization of platelets or plaque debris was considered responsible for most of the remaining micronecroses. During 6month follow-up rates of clinical restenosis (44 vs 9%, p=0.059) tended to be higher in patients with as compared to patients without cTnT release after DCA. Conclusion Successful DCA is associated with postprocedural elevations of cTnT which relate to minor vascular complications and presumably microembolization of platelets or plaque debris. The superior diagnostic performance of cTnT compared to CK-MB mass may relate to more sensitive identification of microinfarction. Further studies are mandatory to confirm the association between elevation of cTnT and risk of restenosis and TVR.     

Serial determinations of serum enzymes following aorta-coronary bypass surgery and acute myocardial infarction

Serial determinations of serum creatine kinase (CK), cardio-specific isoenzyme of CK (CK-MB), glutamic oxaloacetic transaminase (GOT) and alpha-hydroxybutylate dehydrogenase (HBD) were made in 29 consecutive patients undergoing aorta-coronary (AC) bypass grafting, and the results were compared with those in 31 patients with acute myocardial infarction (AMI). Postoperatively, all patients had an uneventful postoperative course and there was no evidence of AMI. The time course of enzyme activity following surgery was characterized by 1) shortening of peak activity time of all enzymes except CK, 2) rapid disappearance of CK-MB, 3) prolonged normalization of GOT and HBD. Peak activities of CK, CK-MB, GOT and HBD in AC bypass patients were 801 +/- 77, 46 +/- 6, 100 +/- 9 and 718 +/- 32 IU (mean +/- SEM), respectively, which were equivalent to 46%, 12%, 22% and 47% of those in AMI. The degree of postoperative CK-MB elevation was influenced by the duration of the operation and the extracorporeal circulation, and the number of grafts bypassed. The peak CK-MB activity did not correlate with the CK peak. The ratio of CK-MB to CK was much smaller in AC bypass than in AMI (6.5 +/- 1.8 vs. 20.1 +/- 1.4%). It was concluded that serum enzyme elevations after AC bypass surgery largely reflected enzyme release from the skeletal muscle rather than the myocardium.     

Pathophysiology of early coronary angioplasty with stenting on non-Q-wave vs Q-wave myocardial infarction

This study was undertaken to evaluate the pathophysiologic and clinical effects of the early application of percutaneous transluminal coronary angioplasty (PTCA) supported by stenting on non-Q-wave myocardial infarction (MI). Ninety-four patients with non-Q-wave MI and 316 patients with Q-wave MI were studied. Early PTCA with provisional stenting (40%) was performed in all of them. A history of MI (22% vs 12%, p=0.018), preinfarction angina < or = 24 hours before the onset of MI (60% vs 33%, p<0.001), and patent infarct-related vessels (83% vs 21%, p<0.001) were significantly more common in non-Q-wave MI than in Q-wave MI. As predictors of the occurrence of non-Q-wave MI, preinfarction angina (p=0.001) and previous MI (p=0.021) were significant variables. Clinical outcomes showed more improvement in in-hospital death (0.0% vs 5.0%, p=0.036) and long-term event-free curves for death and/or MI (p=0.035) in non-Q-wave MI than Q-wave MI when patients with previous MI were excluded. There was no significant difference in clinical outcome between the two groups when patients with previous MI were included. The high incidence of patent infarct-related vessels and preinfarction angina as well as the improved outcome obtained by early PTCA/stenting suggest instability of coronary occlusion and culprit coronary lesions in non-Q-wave MI. In conclusion, non-Q-wave MI constitutes a characteristic feature of MI induced by unstable coronary lesions, and early interventional therapies are presumed to result in improved outcomes by stabilizing the unstable culprit lesions.     

Cardiac event rate after non-Q-wave acute myocardial infarction and the significance of its anterior location

To correlate cardiac event rate with infarct location on the electrocardiogram in patients recovering from a non-Q-wave acute myocardial infarction (AMI), 135 consecutive patients with enzymatically proven non-Q-wave AMI were followed prospectively for a median of 9.9 months. Of these, 65 patients were classified as having had an anterior non-Q-wave AMI, defined as new ST- or T-wave changes, or both, in leads V1 through V4 (group 1). The remaining 70 patients were classified as having had inferior or lateral non-Q-wave AMI, or both, defined as ST- or T-wave changes in 2 consecutive leads (II, II aVF; II and aVL or V5 and V6) (group 2). At baseline group I was older and had a higher incidence of previous AMI than group 2. After adjusting for baseline variables, the patients in group I had a 29% reinfarction and 32% mortality rate, which was significantly higher (p less than 0.002 for both) when compared to group 2, which had a reinfarction and mortality rate of 8 and 9%, respectively. Patients with anterior non-Q-wave AMI are at very high risk for developing a major cardiac event very soon after the index AMI. This high risk is probably related to a larger area of residual ischemic but viable myocardium in the infarct-related artery when compared to inferolateral non-Q-wave AMI.     

Long-term prognosis in relation to ECG findings in acute myocardial infarction

In 680 patients with acute myocardial infarction the prognosis during the following 5 years was related to observations made in a standard electrocardiogram (ECG) and 24 precordial chest leads. Patients with a Q-wave infarction (based on a 12-lead standard ECG) had a mortality rate during hospitalization of 10.2% which was much higher than that in patients with a non-Q-wave infarction (1.9%, p less than 0.001). At 5 years' follow-up 33.6% of those with a Q-wave infarction had died versus 28.4% of those with a non-Q-wave infarction (p greater than 0.2). Corresponding mortality rate among patients with no previous infarction (n = 587) was 32.1% and 25.2%, respectively (p = 0.17). In patients with anterior infarction and no previous infarction there was no correlation between Q- and R-wave changes in the 24 chest leads 4 days after admission to hospital and 5-year mortality rate. We thus conclude that patients with a Q-wave infarction had a higher in-hospital mortality compared with non-Q-wave infarction as judged from standard ECG, whereas 5-year mortality was similar. Similarly, there was no correlation between Q- and R-wave changes in an increased number of chest leads and 5-year mortality rate.     

The appearance of giant negative T waves in anterior acute myocardial infarct with a Q wave is associated with minor myocardial damage and a minor extension of coronary disease]

INTRODUCTION AND OBJECTIVE: The early inversion of T waves in patients with acute myocardial infarction has recently been related to a better left ventricular function and a more favourable evolution, contrary to what happens in the unstable angina. On the other hand, the significance of the appearance of deep negative T waves in the early phase of some acute myocardial infarction is not known. The aim of this study is to evaluate its relation with the existing myocardial damage and the underlying coronary artery disease extension in anterior some with Q wave. METHODS: 48 patients with a first anterior Q-wave acute myocardial infarction, thrombolized or not, admitted to hospital with an evolution of less than 24 hours, and with a coronariography performed before discharge were analyzed. Giant negative T waves were defined as those which were 8 mm or more from baseline. RESULTS: 17 of the 48 patients presented giant negative T waves (T-group) and 31 did not (N-group). In the T-group patients, the size of the negative T wave was 11.29 +/- 2.86 mm and the number of precordial leads with negative T waves was 4.35 +/- 1.57. There were no differences between both groups in variables such as sex, coronary risk factors, and other basal characteristics. The T-group patients were younger, had lower peak-CK, CK-MB and LDH levels and presented greater recovery of R waves during the follow-up, the differences being significant with the N-group patients. The left ventricular ejection fraction was higher (56.3 +/- 13.4 vs 42 +/- 12%; p < 0.001) and the number of affected coronary vessels was lower in the T-group (1.12 vs 1.64; p < 0.01); there were no differences in the localization or severity of coronary lesions, nor in the frequency of postinfarction myocardial angina. None of the patients in the T-group were Killip > I, while this situation occurred in 38.7% of the N-group patients. CONCLUSIONS: The appearance of giant negative T waves in the acute or early phase of Q-wave anterior acute myocardial infarction is associated with a smaller infarct size, lower functional deterioration and less extension of the underlying coronary disease.