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PubMed2001

Incidence, risk factors, and clinical outcome of stroke after acute myocardial infarction in clinical practice. MIR and MITRA Study Groups. Myocardial Infarction Registry. Maximal Individual Therapy in Acute Myocardial Infarction .

In this analysis of ischemic and hemorrhagic strokes after acute myocardial infarction (AMI) in 21,330 consecutively included patients with AMI, we found an incidence of stroke after AMI of 1.2% and a very poor prognosis. Previous stroke, atrial fibrillation, and older age were the strongest predictors of stroke after AMI; thrombolysis was a borderline risk factor and early therapy with aspirin was associated with a reduction in stroke after AMI.

Aged↗
PubMed1993

Residual flow to the infarct zone as a determinant of infarct size after direct angioplasty.

BACKGROUND: In acute myocardial infarction, residual flow to the infarct zone either through antegrade flow in the infarct-related coronary artery or collateral flow from the non-infarct-related arteries is often present before reperfusion therapy. The purpose of this study was to assess the influence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before successful direct angioplasty on infarct size and myocardial salvage in patients with acute evolving myocardial infarction. METHODS AND RESULTS: Sixty patients with acute evolving myocardial infarction underwent direct successful angioplasty without prior thrombolytic therapy. The myocardium at risk of infarction, the final infarct size, and myocardial salvage were measured by tomographic perfusion imaging with 99mTc sestamibi. Antegrade flow in the infarct-related artery before intervention was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study group classification. Collateral flow to the infarct zone before angioplasty was also graded (0 through 3, 0 being no collateral flow). The presence of even minimal antegrade flow before angioplasty (TIMI grade 1) in the infarct-related artery compared with absent flow was associated with a significant reduction in final infarct size (9 +/- 17% versus 23 +/- 19% of left ventricle, P = .02) and a significant increase in myocardial salvage (23 +/- 16% versus 14 +/- 13% of left ventricle, P = .05) after angioplasty. When antegrade flow in the infarct-related artery was absent before angioplasty, the presence of collateral flow before angioplasty resulted in a significantly smaller final infarct size (P = .01) and more myocardial salvage (P = .05) after angioplasty. Both antegrade infarct-related artery flow and collateral flow to the infarct zone had significant independent ability to predict infarct size after angioplasty. When collateral grade and TIMI grade were added to provide an estimate of residual flow, a model including residual flow, myocardium at risk, and the interaction of residual flow and infarct site explained 83% of the variability in infarct size after angioplasty. CONCLUSIONS: The presence of antegrade flow in the infarct-related artery and/or collateral flow to the infarct zone before direct angioplasty in acute evolving infarction results in a smaller infarct size after direct successful angioplasty.

Angioplasty, Balloon, Coronary↗
PubMed1992

Relationships of site of infarction and history of previous infarction with short- and long-term prognosis after acute myocardial infarction in Japan.

We studied the outcome in 308 patients with acute myocardial infarction (MI) admitted to the coronary care unit of Kobe General Hospital. Short-term outcome (within 28 days after MI) and long-term outcome (more than 28 days) were examined with survival curves to find any relationship with a history of previous MI and with the site of the MI. In the short term, 38 of the 308 patients died of cardiac causes. The group with anterior MI tended to have higher mortality than the group of patients with inferior MI, and among patients without a previous MI, patients with anterior MI had significantly higher mortality (p = 0.01). In multivariate analysis by the logistic regression model, the site of the MI was found to be independently associated with the short-term outcome. In the long term, with a mean follow-up of 3.4 years, 23 of the 308 patients died of cardiac causes. Different sites of the MI did not result in different outcomes in patients with or without a previous MI. Of patients with anterior or inferior MI, those with a previous MI tended to have higher mortality, and of patients with an inferior MI, the difference was significant (p = 0.001). In multivariate analysis by the proportional hazards model, a history of MI was more predictive than the site of the MI. In conclusion, the site of the MI was associated more with the short-term outcome than with the long-term outcome, and a history of MI was associated more closely with the long-term outcome.

Aged↗
PubMed1995

Prognosis of patients > or = 70 years of age with non-Q-wave acute myocardial infarction compared with younger patients with similar infarcts and with patients > or = 70 years of age with Q-wave acute myocardial infarction.

In this study, 70 patients > or = 70 years of age admitted to the coronary care unit with non-Q-wave acute myocardial infarction (AMI) were followed prospectively for 1 year, and the clinical course in these patients was compared with that in 61 patients < 70 years with non-Q-wave AMI and 56 patients > or = 70 years with Q-wave AMI. Compared with the younger patients with non-Q-wave AMI, older patients were more likely to develop atrial fibrillation (23% vs 8%; p < 0.05) and congestive heart failure (53% vs 30%; p < 0.01), and less likely to receive thrombolytic therapy (9% vs 28%; p < 0.01), cardiac catheterization (41% vs 72%; p < 0.01), and coronary angioplasty (20% vs 39%; p < 0.05). Hospital mortality did not differ significantly between older and younger non-Q-wave AMI patients (10% vs 3%), but 1-year mortality was higher in the elderly (36% vs 16%; p = 0.02). Elderly patients with Q-wave AMI had more in-hospital complications, including death (25% vs 10%; p < 0.05), than elderly patients with non-Q-wave AMI. In contrast, postdischarge mortality was higher in elderly patients with non-Q-wave AMI, so that total mortality at 1 year was similar in the 2 groups. Overall, elderly patients with non-Q-wave AMI accounted for 62% of all deaths occurring during the first year after discharge (relative risk 2.6 compared with other groups; p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors↗
PubMedDate not supplied

[Enzyme activity in post-infarct aneurysm and in the myocardial zone outside the infarct in experimental infarct in rats].

Activities of lactate dehydrogenase, glucose-6-phosphate dehydrogenase, transketolase and creatine phosphokinase were studied in tissue of aneurysm and in extrainfarctional part of rat heart muscle after experimental infarction. Activity of total LDH, content of its anode isoenzymes and creatine phosphokinase activity were decreased. Enzymes of pentose phosphate pathway were activated and amount of cathode LDH isoenzymes was increased. The most distinct and apparently irreversible alterations in the enzymatic activity were observed in the aneurysm tissues.

Animals↗
PubMed2003

Zonal frequency analysis of infarct extent. Part II: anterior and posterior cerebral artery infarctions.

The object of the study was to test the hypotheses that analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA) infarcts, and by dual- and triple-vessel infarcts, will disclose (i) sites most frequently involved by each infarct type (peak sites), (ii) sites most frequently injured by multiple different infarct types (vulnerable zones), and (iii) anatomically overlapping sites in which the relative infarct frequency becomes equal for two or more different infarct types and/or in which infarct frequency shifts greatly between single and multivessel infarcts (potential border zones). Precise definitions of each vascular territory were adopted. CT and MRI studies from 20 ACA, 20 PCA, three dual ACA-PCA, and four triple ACA-PCA-MCA infarcts were mapped onto a standard template (Part I). Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each infarct type, the zones most frequently affected by multiple different infarct types, the zones where relative infarct frequency was equal for different infarcts, and the zones where infarct frequency shifted markedly from single- to multiple-vessel infarcts. Zonal frequency analysis provided quantitative data on the relative infarct frequency in each anatomic zone for each infarct type. It displayed zones of peak infarct frequency for each infarct, zones more vulnerable to diverse types of infarct, peripheral "overlap" zones of equal infarct frequency, and zones where infarct frequency shifted markedly between single- and multiple-vessel infarcts. It is concluded that the hypotheses are correct.

Adolescent↗
PubMedDate not supplied

Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts.

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenergic beta-Antagonists↗
PubMed1980

[Diagnosis of limited septal infarction associated with a posterior or postero-inferior infarction. Value of vectorcardiography and clinical, coronary angiographic and developed correlations].

In patients with posterior or postero inferior infarction, a limited septal infarction may be detected by vectorcardiography, septal extension being a sign of disease of the left anterior descending artery. In order to confirm this hypothesis, 31 posterior or postero inferior infarction with septal extension were selected by vectorcardiography from more than 500 ECGs recorded after the acute phase of a clinically and biologically documented infarction. The following criteria were chosen: 1. Anterior deviation of the QRS, associated or not with superior deviation of the initial deflection lasting over 25 ms and clockwise rotation of the frontal loop (posterior infarct: 9 cases, postero inferior infarct: 22 cases). 2. Abnormalities of the initial phase of the QRS in the horizontal plane, associated with a reduced amplitude and duration of the initial deflection. The clinical, ECG, vectorcardiographic and angiographic (14 cases) features of these 31 postero septal infarcts were compared with those of 31 posterior septal infarcts were compared with those of 31 posterior or postero inferior infarcts (24 coronary angiographies). 1. From the clinicl point of view, in the acute phase postero septal infarction did not differ from posterior infarction and the early prognosis was favourable. On the other hand, with an average follow-up of 2 years, the outcome of postero septal infarction was statistically more complicated than that of strict posterior infarction (52 p. 100 compared to 19 p. 100, p < 0.01). 2. From the electrocardiographical point of view, septal extension of posterior infarction was only suspected in 25 p. 100 cases. In the acute phase, ST depression in V2 to V5 sometimes associated with reduction of the R wave in the right precordial leads and QS waves in V4R, suggesting a "rudimentary" or "subendocardial" infarct. 3. From the angiographic point of view, although disease of the posterior vessels was equally common in posterior and postero septal infarction (86 p. 100 compared to 92 p. 100 NS), stenosis of the left anterior descending artery was statistically more common in postero septal infarction than in posterior infarction (86 p.100 compared to 29 p. 100, p < 0.001). Thallium myocardial scintigraphy, when performed, showed the double myocardial lesion in the antero septal and postero inferior walls in postero septal infarction. These results validate the vectorcardiographical criteria retained for diagnosis of postero septal infarction and confirmed the superiority of the vectorcardiogramme over the electrocardiogramme in the diagnosis of double infarction. Therefore, the vectorcardiogramme in the diagnosis of double infarction. Therefore, the vectorcardiogramme allows selection of the patients with postero diaphragmatic infarction with a limited septal extension, for whom coronary angiography should be proposed. A "postero septal" infarct diagnosed on vectorcardiogramme has a high probability of stenosis of the left anterior descending artery.

Coronary Angiography↗
PubMed1998

5993 survivors of suspected myocardial infarction. 10 year incidence of later myocardial infarction and subsequent mortality.

AIMS: To evaluate the 10-year incidence of later infarction and subsequent mortality, as well as predictors of later infarction, in patients with suspected myocardial infarction and alive on day 15 after admission. METHODS AND RESULTS: 5993 patients admitted with suspected myocardial infarction and alive on day 15 after admission were registered in The First Danish Verapamil Infarction Trial database in 1979-81. 2586 had definite infarction, 402 probable infarction and 3005 no infarction as they fulfilled 3, 2 and 1 criteria for infarction. They were followed for 10 years with respect to later infarction and death, i.e., including death after later infarction. The 10 year infarction rate after index admission was 48.8% in definite, 47.3% in probable and 24.6% in no infarction patients (P < 0.0001). The subsequent 10-year mortality was 82.3% in primary definite, 74.7% in primary probable, and 77.9% in primary no infarction patients (ns), Cox regression analysis with sex, age group, and definite, probable or no infarction as independent variables showed that females aged < 50 years without a primary infarction had the lowest hazard ratio (0.13 relative to males, aged 50-65 years with definite/probable infarction at index admission) for a later infarction, in contrast to the highest hazard ratio (1.17) for males aged > 65 years with definite or probable infarction. CONCLUSION: The 10-year infarction rate in patients with suspected myocardial infarction in whom the diagnosis is ruled out is lower than in those with definite or probable infarction, but the mortality after a later infarction is similar in all three groups.

Adult↗
PubMed1992

Biomechanical properties of reperfused transmural myocardial infarcts in rabbits during the first week after infarction. Implications for left ventricular rupture.

Left ventricular (LV) rupture potential was studied after transmural myocardial infarction (MI) in rabbits by measuring 1) the tensile strength of infarcted tissue strips, 2) the force required to initiate a tear (tear threshold) in the central infarcted region, and 3) the intracavitary pressure required to rupture the infarcted ventricle. During the first week after MI, infarcts resulting from a permanent coronary occlusion were compared with infarcts reperfused "late" (i.e., 3 hours) after coronary occlusion with a resultant hemorrhagic transmural infarct but no reduction in infarct size. The reperfused hemorrhagic infarcted strips had less tensile strength than strips from permanently occluded infarcts in the initial 24 hours after MI (16 +/- 1 versus 24 +/- 3 g/mm2, p less than 0.05), but the tear threshold and response to increased LV pressure were not influenced by infarct reperfusion at this time. By 3 days after MI, reperfused infarcts had equal tensile strength, had greater resistance to infarct tearing, and could withstand a greater LV distending pressure compared with permanently occluded infarcts. By 5 days after MI, reperfused infarcts maintained a greater tear threshold but had less tensile strength than permanently occluded infarcts, although all infarct values were equivalent or greater than normal LV values. By 7 days after MI, reperfused and permanently occluded infarcts were equally strong by all measurements. Thus, late reperfusion of transmural infarcts increased resistance to infarct tearing and LV rupture above that of nonreperfused permanently occluded infarcts by 3 days after MI and enhanced tissue strength after an initial 24-hour vulnerable period. These findings suggest that late reperfusion may accelerate myocardial healing after MI.

Animals↗
PubMed1981

Nontransmural myocardial infarction: a comparison of hospital and late clinical course of patients with that of matched patients with transmural anterior and transmural inferior myocardial infarction.

The hospital and long-term course of 67 patients with nontransmural myocardial infarction was compared with that of 66 patients with transmural anterior and 63 patients with transmural inferior infarction matched for age, sex, previous infarction and prior congestive heart failure. During their hospital stay, patients with nontransmural infarction had significantly less congestive heart failure and fewer intraventricular conduction defects than did patients with transmural anterior infarction; fewer atrial tachyarrhythmias and less sinus bradycardia and atrioventricular block than did patients with transmural inferior infarction; and an incidence of hypotension, pericarditis and ventricular irritability similar to that of patients in the other two groups. Patients with nontransmural infarction had a significantly lower coronary care unit mortality rate (9 percent) than that of patients with transmural anterior or transmural inferior infarction (20 and 19 percent, respectively). By 3 months, the mortality rate had risen to 14 percent in patients with nontransmural infarction, but was significantly higher (29 and 27 percent, respectively) in patients with transmural anterior or transmural inferior infarction. Angina was common in all three groups, occurring in more than 50 percent of patients during a mean follow-up period of 28.6 months after hospital discharge. In contrast, the incidence of subsequent myocardial infarction was significantly greater in patients with nontransmural myocardial infarction, occurring in 21 percent at 9 months compared with only 3 percent of patients with transmural anterior (p less than 0.01) and 2 percent of patients with transmural inferior (p less than 0.05) infarction. By 54 months, 57 percent of patients with nontransmural infarction had sustained a new infarction contrasted with only 12 percent of patients with transmural anterior (p less than 0.001) and 22 percent of patients with transmural inferior (p less than 0.01) infarction. Late mortality increased in patients with nontransmural myocardial infarction and, although this group had a significantly better survival rate at 3 months, the overall late mortality of the three groups was comparable. The study suggests that nontransmural myocardial infarction is an unstable ischemic event associated with a great risk of later myocardial infarction and high late mortality rate. A more aggressive diagnostic and therapeutic approach may be warranted in patients with nontransmural myocardial infarction.

Arrhythmias, Cardiac↗
PubMed2000

Atherothrombotic middle cerebral artery territory infarction: topographic diversity with common occurrence of concomitant small cortical and subcortical infarcts.

BACKGROUND AND PURPOSE: MRI has superior capabilities for the detection of cerebral infarcts compared with CT. CT was used to locate infarcts in most previous studies of atherothrombotic middle cerebral artery (MCA) territory infarcts. Thus, there was a possibility of missing concomitant small infarcts. More accurate identification of topographic lesions in MCA territory with MRI may help to establish the pathogenesis of stroke. The present study determines topographic patterns, distribution of vascular lesions, and probable mechanisms. METHODS: Forty-two patients with MCA territory infarcts on routine MRI and no major cause of cardioembolism were studied with conventional angiography or MR angiography. RESULTS: The topographic patterns seen on MRI were subdivided into 4 groups: cortical border-zone infarcts (n=6), pial territory infarcts without insular infarct (n=3), pial territory infarcts with insular infarct (n=14), and large subcortical infarcts (n=19). Of 6 patients with cortical border-zone infarcts, 4 had concomitant small cortical or subcortical multiple lesions. Angiography showed intrinsic MCA disease in 4 patients. Of 3 patients with pial territory infarcts without insular infarct, 2 also had small multiple centrum ovale lesions. All had intrinsic MCA disease. Pial territory infarcts with partial or whole insular lesions were present in 10 and 4 patients, respectively. Five patients had additional multiple cortical or subcortical lesions. Ten patients had intrinsic MCA disease. Of the 19 patients with large subcortical infarcts, 12 had centrum ovale infarcts, and 4 had both basal ganglia and centrum ovale lesions. Ten had concomitant small cortical or subcortical lesions. Six patients had intrinsic MCA disease. CONCLUSIONS: Similar vascular lesions induce different topographic patterns in MCA territory infarction, which are related to individual vascular variability, degree of primary and secondary collateralization, and pathogenesis of infarcts. Our study indicates that concomitant small cortical or subcortical lesions are also commonly associated findings in diverse patterns of MCA territory infarction, which can mostly be explained by probable embolic mechanism.

Adult↗
PubMed1995

Relation of initial infarct size to extent of left ventricular remodeling in the year after acute myocardial infarction.

OBJECTIVES: This study attempted to determine the relation between infarct size after acute myocardial infarction and subsequent left ventricular remodeling using precise clinical measurements. BACKGROUND: Animal studies have demonstrated that the degree of left ventricular remodeling after myocardial infarction is linearly related to infarct size. Clinical studies have not clearly replicated these results because of imprecise measurements and failure to adjust for patency of the infarct-related artery. METHODS: Infarct size was measured from technetium-99m (Tc-99m) sestamibi perfusion images in 14 patients (12 with an anterior, 2 with an inferior infarction) by a threshold method previously described and expressed as percent of the left ventricle (32 +/- 17% left ventricle [mean +/- SD], range 6% to 58%). Absolute end-systolic volume, end-diastolic volume and ejection fraction were determined by electron beam computed tomographic images performed at discharge and at 6 weeks, 6 months and 1 year after myocardial infarction. All patients had documented infarct-related artery patency after reperfusion therapy. RESULTS: At hospital discharge, there was no correlation between infarct size and end-systolic and end-diastolic volumes or ejection fraction. There was significant left ventricular dilation in the study group over the next year. As remodeling progressed, there was closer correlation between infarct size and ejection fraction and end-systolic volume measures (infarct size vs. end-systolic volume, from r = 0.43 at discharge to r = 0.80 at 1 year; infarct size vs. ejection fraction, from r = -0.39 at discharge to r = -0.84 at 1 year). There was a strong inverse correlation between infarct size at discharge and subsequent changes over the next year in end-systolic volume (r = 0.63, p = 0.02) and ejection fraction (r = -0.66, p = 0.01). CONCLUSION: Infarct size as measured by Tc-99m sestamibi at hospital discharge after an index infarction is predictive of subsequent change in left ventricular volume and function in the year after myocardial infarction. Patients with a large infarct demonstrated the greatest degree of dilation in the setting of patency of the infarct-related artery.

Adult↗
PubMed2002

[Quantitative assessment of acute myocardial infarction size. Impact of early mechanical recanalization of infarct related artery].

UNLABELLED: The aim of investigation: 1) to determine the diagnostic value of QRS score and LV echocardiography in assessment of the size of myocardial infarction in acute stage, 2) to establish the impact of infarct related artery recanalization on myocardial infarction size. METHODS AND MATERIAL: In order to investigate whether infarct size could be estimated by QRS scoring system soon after reperfusion we evaluated QRS score obtained serially before and twice after reperfusion, and the echocardiographic global EF in 57 patients with acute myocardial infarction who underwent successful mechanical recanalization of infarct related artery. Coronary flow in infarct related artery was evaluated by the Thrombolysis in Myocardial Infarction trial (TIMI) criteria. QRS scores were calculated according to the method of Wagner (37 criteria and 29 points). The electrocardiographic ejection fractions (EFECG) were calculated according to Roubin method, and the global echocardiographic ejection fractions (EFECHO) were calculated according to Simpson method. All patients were divided into 3 groups according to the quality of myocardial reperfusion expressed as intensity in change of electrocardiographic phases at the time of infarct related artery recanalization (1 gr.--the change of ECG phases > or = 2; 2 gr.--the change of ECG phases through 1; and 3 gr.--with no changes of ECG stages). All patients had an effective infarct-related artery recanalization expressed as 2 or 3 TIMI grade. RESULTS: A low and insignificant correlation was observed between EFECG and EFECHO for patients with anterior myocardial infarction (r = 0.35) and for patients with posterior myocardial infarction (r = 0.12). The EFECG had a tendency to be lower in patients with worse myocardial reperfusion (from 59.06 +/- 6.12 in 1 gr. to 50.93 +/- 10.87 in 3 gr). At this time the EFECHO was almost the same in all groups of patients. Additionally, the EFECHO was significantly lower than EFEKG in all groups of patients (p = 0.000017-0.001). The QRS score had general tendency to increase after infarct-related artery recanalization, however the most evident increase was obtained in 1 gr. of patients with rapid change of ECG stages. A significant correlation (r = 0.87 for patients with anterior myocardial infarction and r = 0.85 for patients with posterior myocardial infarction) was observed between QRS scores obtained after infarct related artery recanalization and that obtained after 10-12 days. In conclusion, QRS score and EFEKG better than EFECHO reflects the myocardial infarction size in acute stage. Increasing of the myocardial infarction size after infarct-related artery recanalization is connected with reperfusional injury more expressed in patients with more effective myocardial reperfusion.

Adult↗
PubMed1992

Modifiers of timing and possible triggers of acute myocardial infarction in the Thrombolysis in Myocardial Infarction Phase II (TIMI II) Study Group.

OBJECTIVES: The aim of this study was to provide insight into the mechanism of acute myocardial infarction by determining the modifiers of timing and possible triggers of onset of infarction. BACKGROUND: A higher frequency of onset of acute myocardial infarction has been reported in the morning with a peak in the 1st 3 h after awakening. This observation suggests that the onset of infarction may be triggered by activity in the morning and at other times of the day. METHODS: The clinical history of the 3,339 patients entered into the Thrombolysis in Myocardial Infarction phase II study was analyzed to determine characteristics predicting a higher frequency of infarction between 6 AM and noon, and onset of infarction during exertion. RESULTS: A higher proportion (34.4%) of infarctions began in the morning (6 AM to noon) compared with other times of the day. Characteristics independently predicting a higher frequency between 6 AM to noon were no beta-adrenergic blocking agent use in the 24 h before infarction, no discomfort other than the index pain in the preceding 48 h, occurrence of the infarction on a weekday and no history of current smoking. In 18.7% of patients, infarction occurred during moderate or marked physical activity. Independent predictors of exertion-related infarction included male gender, no history of current smoking, white race, no use of calcium channel blocking agents or nitrates in the preceding 24 h, the absence of either chest pain at rest in the 3 weeks before infarction or any pain in the preceding 48 h, the absence of new onset angina and the presence of exertional pain in the preceding 3 weeks. Compared with patients whose infarction occurred at rest or during mild activity, those with exertion-related infarction had fewer coronary vessels with > or = 60% stenosis (p = 0.002) and were more likely to have an occluded infarct-related vessel after thrombolytic therapy (p = 0.01). CONCLUSIONS: Further study of the timing and activity at onset of infarction may provide insight into the pathophysiologic mechanisms causing acute myocardial infarction and provide clues to preventive measures.

Analysis of Variance↗
PubMed1986

Healing after myocardial infarction in the dog: changes in infarct hydroxyproline and topography.

Temporal changes in infarct collagen and left ventricular topography during healing after myocardial infarction were studied in 132 dogs with coronary artery ligation: 8 sham dogs and 13 with no infarction (controls) and 111 with infarction (3 at 1 day, 54 at 2 days, 25 at 7 days, 3 at 2 weeks, 9 at 4 weeks and 17 at 6 weeks). Myocardial hydroxyproline (a marker of collagen) was measured by spectrophotometry and pathologic infarct size, arteriographic occluded bed size and topography by computerized planimetry of weighed left ventricular rings. Over 6 weeks, hydroxyproline was unchanged in normal regions (average 4.20 mg/g dry weight) but increased progressively between 7 days and 6 weeks (9.94 versus 55.55 mg/g, p less than 0.001) in infarct zones. Progressive infarct contraction occurred over 6 weeks, with infarct size at 6 weeks being 40% less than at 2 days (9.7 versus 16.3% of the left ventricle, p less than 0.001), although total infarct hydroxyproline was directly related to infarct size at each time period (r = 0.73 to 0.81, p less than or equal to 0.05). Significant (p less than or equal to 0.05) left ventricular topographic changes in infarct hearts compared with control hearts included: 1) increase in cavity area (5.0 versus 3.9 cm2), endocardial circumference (8.8 versus 7.4 cm) and expansion index (infarct/normal endocardial segment length, 1.21 versus 1.02) by 7 days; and 2) decrease in thinning ratio (infarct/normal wall thickness, 0.71 versus 0.98) by 6 weeks. Also, compared with 2 day infarcts, by 6 weeks infarct area was decreased (1.8 versus 3.4 cm2) and the noninfarcted segment length increased (6.9 versus 5.4 cm). Changes in hydroxyproline and topography were similar for anterior (n = 54) and posterior (n = 57) infarcts. Thus, healing in canine infarcts is associated with cavity dilation and infarct expansion within 7 days followed by infarct contraction and thinning by 6 weeks, whereas collagen increases between 7 days and 6 weeks. Collagen deposition in expanded and thinned infarct segments explains the permanent regional shape distortion associated with ventricular aneurysms.

Animals↗
PubMed1988

Location of an acute myocardial infarct in patients with a healed myocardial infarct: analysis of 129 patients studied at necropsy.

To determine the relation of a single healed myocardial infarct to a fatal acute myocardial infarct, 129 patients with 1 grossly visible healed and 1 grossly visible acute infarct were studied at necropsy. It was determined whether the acute infarct was opposite to or adjacent to the healed infarct or if 1 infarct was so large that it was both opposite to and adjacent to the other infarct. In 74 (57%) of the 129 patients, the 2 infarcts were opposite one another, in 40 (31%) they were adjacent and in 15 (12%) they were both opposite and adjacent. The age, sex, mean size of the healed infarct and heart weight were similar among the 3 groups. Acute myocardial infarcts were larger in the group that had both opposite and adjacent infarcts than either of the other 2 groups (p less than 0.001). Information regarding whether the infarcts were clinically recognized or not was available in 108 patients: both infarcts were recognized in 41 (38%), neither infarct was recognized in 15 (14%) and 1 infarct was recognized and the other was not in 52 (48%). The number of the 4 major epicardial coronary arteries narrowed at some point greater than 75% in cross-sectional area by atherosclerotic plaque was similar in patients with recognized and in those with unrecognized infarcts. Similar numbers of narrowed major epicardial coronary arteries also were found in each of the 3 infarct groups (opposite, adjacent or both).

Acute Disease↗
PubMed1996

Acute and long-term effects of thrombolysis after anterior wall acute myocardial infarction with serial assessment of infarct expansion and late ventricular remodeling.

This study investigates the impact of thrombolysis on infarct expansion and subsequent left ventricular (LV) remodeling in patients with anterior wall acute myocardial infarction (AMI). We evaluated 51 consecutive patients (24 treated with thrombolysis) with anterior wall AMI by 2-dimensional echocardiography in the following sequence: days 1, 2, 3, and 7, after 3 and 6 weeks, and after 3, 6, and 12 months. LV end-diastolic and end-systolic volume indexes were determined from apical 2- and 4-chamber views using Simpson's biplane formula. Infarct and total LV perimeters were determined in the same views and their ratio expressed as infarct percentage. Infarct expansion was defined as: (1) an increase in infarct percentage and total perimeter >5% on days 2 to 3 in either of the views, or (2) initial infarct percentage >50% with an increase in total perimeter >5% on days 2 to 3. Coronary angiography was performed in 43 patients before discharge, and patency of the infarct-related artery was assessed using Thrombolysis in Myocardial Infarction trial criteria. Infarct expansion was detected in 23 patients. Infarct perimeter steadily decreased in patients with versus without thrombolysis and in patients with patent versus occluded infarct-related arteries. Furthermore, by logistic regression, thrombolysis (p = 0.007) and potency of the infarct-related artery (p = 0.02) were strong negative predictors of expansion, whereas initial infarct perimeter (p = 0.009) was directly associated with subsequent expansion. End-systolic volume index was higher in patients with expansion from day 1 (p = 0.003) through the end of the study (p = 0.021), and end-diastolic volume index was higher in these patients from day 2 (p = 0.012) through 12 months (p = 0.015). Thus thrombolysis, initial infarct size, and infarct-related artery patency are major predictors of infarct expansion after anterior wall AMI.

Confounding Factors, Epidemiologic↗