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PubMed2003

Zonal frequency analysis of the gyral and sulcal extent of cerebral infarcts. Part III: Middle cerebral artery and watershed infarcts.

We tested the hypothesis that frequency analysis of the anatomic zones affected by single anterior (A), posterior (P), and middle (M) cerebral artery (CA), multivessel, and watershed infarcts will disclose specific sites (peak zones) most frequently involved by each type, sites most frequently injured by multiple different types (vulnerable zones), and overlapping sites of equal relative frequency for two or more different types of infarct (equal frequency zones). We adopted precise definitions of each vascular territory. CT and MRI studies of 50 MCA, 20 ACA-MCA, three PCA-MCA, and 30 parasagittal watershed infarcts were mapped onto a standard template. Relative infarct frequencies in each zone were analyzed within and across infarct types to identify the centers and peripheries of each, vulnerable zones, and equal frequency zones. These data were then correlated with the prior analysis of 47 ACA, PCA, dual ACA-PCA, and ACA-PCA-MCA infarcts. Zonal frequency data for MCA and watershed infarcts, the sites of peak infarct frequency, the sites of vulnerability to diverse infarcts, and the overlapping sites of equal infarct frequency are tabulated and displayed in standardized format for direct comparison of different infarcts. This method successfully displays the nature, sites, and extent of individual infarct types, illustrates the shifts in zonal frequency and lesion center that attend dual and triple infarcts, and clarifies the relationships among the diverse types of infarct.

Aged↗

PubMed1986

Effects of early intracoronary streptokinase on infarct size estimated from cumulative enzyme release and on enzyme release rate: a randomized trial of 533 patients with acute myocardial infarction.

The effects of early intracoronary streptokinase (SK) on enzymatic infarct size and rate of enzyme release were studied in a randomized multicenter trial. A total of 533 patients with acute myocardial infarction (AMI) were allocated to either the SK treatment group (n = 269) or the conventional (control) treatment group (n = 264). Enzymatic infarct size was represented by the cumulative quantity of alpha-hydroxybutyrate dehydrogenase (HBDH) released by the heart per liter of plasma in the first 72 hours. Rate of enzyme release was represented by the ratio of HBDH quantities released in 24 hours and 72 hours. On an "intention to treat" basis, the SK group had a smaller (by 30%; p = 0.0001) median enzymatic infarct size and a higher (by 35%; p = 0.0001) median rate of enzyme release than the control group. Limitation of infarct size was less apparent in patients treated with intracoronary SK only (25%) than in patients treated with intravenous plus intracoronary SK (34%). Compared to the control group, the enzyme release rate in patients treated with intracoronary SK only was slightly less (34%) than that in patients treated with intravenous plus intracoronary SK (38%). Patients with a patent infarct-related coronary artery at acute angiography had a median infarct size which was 55% (p = 0.0001) smaller than the median infarct size of the control group, and the median rate of enzyme release was 38% (p = 0.001) higher than the median release rate of the control group. Patients with successful recanalization during intracoronary SK infusion had a median infarct size which was 31% (p = 0.002) smaller than the median infarct size of the control group and a median rate of enzyme release which was 42% (p = 0.0001) higher than the median release rate of the control group. Patients with persistent coronary occlusion in spite of thrombolytic therapy had a median infarct size which was 11% (NS) higher than the median infarct size of the control group, although the median rate of enzyme release was still 23% (p = 0.02) higher than the median release rate of the control group. It is concluded that thrombolysis in the early phase of AMI limits infarct size and that intracoronary SK treatment itself accelerates the process of enzyme release from infarcted myocardium, independent of the angiographic result.

Clinical Trials as Topic↗

PubMed1987

Nausea and vomiting during acute myocardial infarction and its relation to infarct size and location.

Nausea and vomiting occurring during myocardial ischemia is believed to be associated with inferior wall infarction. However, data supporting such an association are limited, and an alternative hypothesis that cardiac vomiting is related to infarct size has also been advanced. The 2 hypotheses were tested in a cross-sectional study of 265 patients consecutively admitted to the coronary care unit. Nausea or vomiting was a good predictor of myocardial infarction (p less than 0.0001). The odds of having an infarction was 3.14 times greater for patients with nausea or vomiting than for those without these symptoms. Nausea was not a good predictor for inferior wall infarction (p = 0.14): 51% of patients with inferior infarcts had nausea or vomiting and 66% with anterior infarcts had these symptoms. Using peak serum creatine kinase level as an index of infarct size, nausea or vomiting was a good predictor of larger infarction. While 55% of all patients with infarction had nausea or vomiting, for patients with infarctions that produced a peak creatine kinase level of more 1,000 IU/liters, 78% had nausea or vomiting. Sex was a marginally important variable. After adjusting for sex, the presence of nausea or vomiting still predicted infarct size (p less than 0.001). Thus, cardiogenic nausea and vomiting are associated with larger myocardial infarctions but do not suggest infarcts in a particular location.

Creatine Kinase↗

PubMed1994

Frequency of chronic obstructive airways disease and pulmonary hypertension in patients with acute inferior myocardial infarction with or without right ventricular infarction.

OBJECTIVE: Factors influencing the incidence of right ventricular infarction among patients with acute inferior myocardial infarction have not yet been fully established. Chronic obstructive airways disease and right ventricular hypertrophy were suggested as possible predisposing factors but no definite evidence was shown. This study analyses the frequency of chronic obstructive airway disease and of Doppler assessed pulmonary hypertension among patients with acute inferior myocardial infarction with or without right ventricular infarction. DESIGN AND PATIENTS: Sixty consecutive patients with acute inferior myocardial infarction were prospectively enrolled into the study. MEASUREMENTS: Standard 12-lead ECG with right precordial leads (V3-6R) were recorded on admission to the Coronary Care Unit and on days 2 and 3. Doppler echocardiography was performed within 48 h after the onset of myocardial infarction and repeated 6 weeks later together with a pulmonary function test. Routine biochemical and clinical data were collected. RESULTS: Right ventricular infarction occurred in 35% of patients with acute inferior myocardial infarction. No differences in respiratory indices of chronic obstructive airways disease or in Doppler echocardiography parameters of pulmonary hypertension were revealed among patients with and without right ventricular infarction. Peak total creatine kinase level and creatine kinase myocardial isoenzyme levels were higher in patients with right ventricular infarction than in those without (2925 +/- 1321 vs. 1682 +/- 1216 U/l; P < 0.001 and 207 +/- 108 vs. 127 +/- 102 U/l; P < 0.05, respectively). CONCLUSIONS: In the course of acute inferior myocardial infarction, the frequencies of chronic obstructive airways disease and/or pulmonary hypertension were not higher among patients with right ventricular infarction than among those without right ventricular infarction. Thus, history of chronic obstructive airways disease and/or pulmonary hypertension do not necessitate specific precautions in respect of right ventricular infarction.

Aged↗

PubMed1989

Functional relation between infarct thickness and regional systolic function in the acutely and subacutely infarcted canine left ventricle.

Specific information regarding the relation between infarct thickness and regional systolic function is important to the overall understanding of both the pathophysiology of acute and subacute myocardial infarction and the functional benefits of myocardial salvage interventions designed to limit the transmural extent of infarction and thereby preserve left ventricular function. In the present study, quantitative computer-assisted two-dimensional echocardiography was used to define the relation between infarct thickness and systolic function in the acutely and subacutely infarcted canine left ventricle. Echocardiograms were obtained at the mid-papillary muscle level at baseline and 6 h after occlusion (acute infarction) in eight animals and at baseline and 72 h after occlusion (subacute infarction) in nine animals. Systolic function was assessed by measuring the extent of fractional radial shortening along each of 36 evenly spaced endocardial targets from end-diastole to end-systole; the transmural extent of infarction was determined from the triphenyltetrazolium chloride-staining deficit at 6 and 72 h. The relation between systolic function and transmural extent of infarction was analyzed in two ways. First, the extent of fractional radial shortening in each group was examined as a function of quartile (25%) increments in transmural infarct thickness. This analysis revealed 1) a significant overall loss of fractional radial shortening with increasing transmural extent of infarction in both groups; and 2) significant differences in the extent of systolic dysfunction between successive quartile increments of infarction. Second, the relation between infarct thickness and systolic dysfunction was modeled mathematically by fitting the data from each infarct series to linear, logarithmic and exponential functions.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Impact of early perfusion status of the infarct-related artery on short-term mortality after thrombolysis for acute myocardial infarction: retrospective analysis of four German multicenter studies.

OBJECTIVE: This study evaluated the impact of early patency of the infarct-related vessel on short-term mortality after thrombolysis for acute myocardial infarction. BACKGROUND: Different thrombolytic regimens for acute myocardial infarction proved to be equally effective in large scale mortality trials despite significant differences in their efficacy with respect to early infarct-related vessel patency as shown in smaller angiographic trials. METHODS: Patients from four German multicenter studies of thrombolysis in acute myocardial infarction were retrospectively evaluated. Of 939 patients with acute myocardial infarction (duration of symptoms < 6 h) treated with thrombolysis, 907 (96.6%) had an angiogram of the infarct-related artery 90 min after the initiation of thrombolytic therapy. The perfusion status was graded according to the Thrombolysis in Myocardial Infarction (TIMI) study criteria. RESULTS: Complete reperfusion (TIMI grade 3) was found in 561 of 907 patients and partial reperfusion (TIMI grade 2) in 122 of 907. Overall, the in-hospital mortality rate was 4.6% (43 patients). In patients with complete reperfusion of the infarct-related vessel, the mortality rate was only 2.7% versus 7.1% in patients with an occluded vessel at the 90-min angiogram. This difference was highly significant in univariate as well as in multivariate analysis. In patients with partial perfusion of the infarct vessel, the mortality rate was 6.6%. CONCLUSIONS: The early perfusion status of the infarct-related artery is an independent predictor of short-term survival. However, only complete early reperfusion is associated with a reduced in-hospital mortality rate whereas patients with partial perfusion (TIMI grade 2) have a short-term prognosis similar to that of patients with persistently occluded infarct vessels. Therefore, when used as a surrogate end point for mortality, only TIMI grade 3 perfusion of the infarct vessel should be interpreted as a treatment success of thrombolysis in acute myocardial infarction.

Adult↗

PubMed1988

Significance of pre-infarction angina for occurrence of post-infarction angina.

We evaluated the factors determining the occurrence of post-infarction angina in 41 patients who had intra-coronary thrombolysis within 6 h of the onset of acute myocardial infarction. Pre-infarction angina was considered to be present if it occurred more than one week before acute myocardial infarction. Post-infarction angina was defined as typical chest pain occurring within 10 days following the infarction. Collateral flow to the infarct zone was determined to be present if any portion of the infarct-related epicardial artery or side branches was visualized. In cases of successful thrombolysis, the prevalence of post-infarction angina was not significantly influenced by pre-infarction angina and the extent of collateral circulation. However, in patients without recanalization, pre-infarction angina and collateral blood flow supply to the area at risk caused a high prevalence of angina after infarction. It is concluded that pre-infarction angina indicative of myocardial ischemia is associated with post-infarction angina especially in patients with conventional therapy, because the jeopardized myocardium is salvaged substantially by collateral circulation with a limited flow reserve.

Adult↗

PubMed1983

Reduction of infarct size in patients with inferior infarction with intravenous glyceryl trinitrate. A randomised study.

Glyceryl trinitrate was previously said to be contraindicated in patients with acute myocardial infarction. Its intravenous administration during acute infarction, however, was associated with a beneficial effect as determined by ST segment mapping. Most recently in a selected group of patients with acute infarction and abnormal haemodynamics, intravenous glyceryl trinitrate was shown to reduce infarct size estimated by enzymes. The present study was performed to verify the safety of intravenous glyceryl trinitrate in patients with infarction under conventional clinical conditions without invasive monitoring and to determine its effect on infarct size in a prospective randomised trial involving 85 patients with infarction (43 treated and 42 control). Treated patients received glyceryl trinitrate within 10 hours of the onset of symptoms (mean 6.0 hours), and the dose was titrated to preset limits for changes in heart rate and blood pressure. In patients with inferior infarction, infarct size estimated by enzymes in the treated was only 12.2 +/- 1.8 versus 19.1 +/- 3.6 CK gram equivalents per metre squared in the placebo group. A similar but statistically insignificant trend was observed for subendocardial infarction but no difference was observed for anterior infarction. Ventricular arrhythmias determined from 24 hour tapes were more frequent in treated patients though this was not statistically significant. Lignocaine requirements in treated and control (1692 +/- 250 vs 1512 +/- 232 mg/24 h) were similar, as were the requirements for morphine (11.4 +/- 1.8 vs 12.2 +/- 2.2 mg/24 h). Results indicate that intravenous glyceryl trinitrate can be administered safely during evolving infarction without invasive monitoring and reduces infarct size in patients with inferior infarction.

Adult↗

PubMed1986

Influence of infarct artery patency on the relation between initial ST segment elevation and final infarct size.

Thirty seven patients with acute myocardial infarction were studied to determine the effect of perfusion of the infarct artery on the relation between the extent of initial ST segment elevation and final electrocardiographic infarct size. The sum of the initial peak ST elevations in all leads correlated with electrocardiographic infarct size in patients with anterior infarction and total occlusion of the infarct artery without collaterals. In patients with anterior infarction and subtotal occlusion of the infarct artery and in all patients with inferior infarction, infarct size was smaller than predicted from the extent of initial ST segment elevation. Collaterals to the infarct artery were present in eight of the 10 patients with inferior infarction and total occlusion. In patients with a persistently occluded infarct artery without collaterals the final infarct size correlated with the extent of initial peak ST segment elevation. This study provides further evidence that spontaneous reperfusion by anterograde flow or via collaterals may salvage jeopardized myocardium.

Adult↗

PubMed1987

Global and regional right ventricular function after acute myocardial infarction: dependence upon site of left ventricular infarction.

The relation of global and regional right and left ventricular function during the acute phase after a first myocardial infarction was assessed by first pass radionuclide angiography in 20 patients (10 after anterior and 10 after inferior myocardial infarction). The right ventricular ejection fraction did not differ significantly between the groups, but left ventricular ejection fraction was significantly depressed after anterior myocardial infarction. There was evidence of right ventricular dilatation and impaired transit in the group with inferior infarction. Five patients with anterior infarction and six with inferior infarction had abnormal right ventricular ejection fractions. Right ventricular wall motion abnormalities affected the septal wall in the group with anterior infarction and the free wall in the group with inferior infarction. The relation between right and left ventricular ejection fractions was markedly different in the two groups. In the group with anterior infarction there was a significant linear relation between right and left ventricular ejection fraction, whereas in the group with inferior infarction there was not. Thus right ventricular dysfunction commonly occurs after both anterior and inferior myocardial infarction. Right and left ventricular impairment are related after anterior myocardial infarction, but are independent after inferior myocardial infarction. Finally, the different effects of anterior and inferior myocardial infarction on right ventricular function may be explained by differences in septal and free wall involvement.

Adult↗

PubMed1977

Correlation of postmortem anatomic findings with electrocardiographic changes in patients with myocardial infarction: retrospective study of patients with typical anterior and posterior infarcts.

This retrospective study correlates electrocardiographic and histopathologic findings in 24 patients with single well-circumscribed infarcts to determine 1) whether ECG terms commonly used to describe the location of myocardial infarcts are significant, and 2) whether the extent of infarct can be determined using QRS characteristics. Transverse sections of the hearts were photographed. Based on histologic sections, the infarct was outlined on the photograph and each section was planimetered via a sonic digitizer into a computer that was programmed to divide the left ventricle into 8 radial sectors and also into basal, mesial, and apical thirds. The percentage of infarct in each of these areas was then calculated. Of the 24 hearts evaluated 12 had posterior infarcts and 12 had anterior infarcts. Posterior infarcts principally involved the basal and mesial levels, whereas the anterior infarcts were more extensive in the apical and mesial thirds, with relative or total sparing of the base. Posterior infarcts were associated with Q waves in leads II, III and aVF in 11 instances. The other posterior infarct was associated with markedly diminished R waves in leads II, III and aVf in the presence of a horizontal axis. All anterior infarcts were associated with Q waves or markedly diminished R waves in the right precordial leads. Eight of the anterior infarcts exhibited circumferential apical involvement and all eight were associated with Q waves or markedly diminished R waves in the left precordial leads. This study documents the electrocardiographic identification of anterior, posterior, and apical infarcts by correlation with pathologic anatomy.

Adult↗

PubMed1991

Influence of coronary collateral vessels on myocardial infarct size in humans. Results of phase I thrombolysis in myocardial infarction (TIMI) trial. The TIMI Investigators.

BACKGROUND: The influence of coronary collateral vessels on infarct size in humans remains controversial, partly because no previous study has examined the impact of collaterals present at the onset of acute myocardial infarction on infarct size. METHODS AND RESULTS: The present study used the data base of the Thrombolysis in Myocardial Infarction (TIMI) Phase I trial to correlate the presence or absence of angiographically documented collaterals in the initial hours of myocardial infarct evolution with the size of the infarct as assessed by serial measurements of serum creatine kinase (CK). To avoid the confounding effects of reperfusion on enzymatic estimates of infarct size, this report is limited to those 125 patients who failed to recanalize at 90 minutes after administration of tissue plasminogen activator or streptokinase. Patients with angiographically documented collaterals (group A, n = 51) had significantly lower values of peak serum CK than patients without collaterals (group B, n = 74) (1,877 +/- 216 versus 2,661 +/- 212 IU/l, respectively [mean +/- SEM], p = 0.004). Similarly, CK-derived infarct size estimates were significantly lower in group A than in group B (20.6 +/- 2.5 versus 31.4 +/- 2.8 CK gram equivalents, p = 0.001). The infarct size observed in patients with collaterals was less for anterior infarctions as well as for infarctions of other locations; thus, the beneficial effects of collaterals were independent of the site of the infarct. In 65 of the 125 patients who failed to reperfuse, left ventricular ejection fraction (LVEF) was assessed by contrast ventriculography both at initial cardiac catheterization (before thrombolytic therapy) and at hospital discharge. Among the patients who had both studies, global LVEF tended to increase from pretreatment to hospital discharge in group A (from 50.6 +/- 1.8% to 53.4 +/- 1.8%, p = 0.10) but decreased in group B patients (from 50.3 +/- 1.8% to 47.8 +/- 1.7%, p = 0.02). At hospital discharge, global LVEF was greater in patients with coronary collaterals (53.5 +/- 1.7% versus 49.6 +/- 1.7%, p = 0.01). CONCLUSIONS: The results demonstrate that, in patients in whom thrombolytic therapy fails to induce reperfusion, the presence of coronary collateral vessels at the onset of myocardial infarction is associated with limitation of infarct size as assessed enzymatically and with improved ventricular function on discharge as assessed by LVEF.

Collateral Circulation↗

PubMed1991

Ten-year incidence of myocardial infarction and prognosis after infarction. Department of Veterans Affairs Cooperative Study of Coronary Artery Bypass Surgery.

BACKGROUND: The 10-year incidence of myocardial infarction (fatal and nonfatal) and the prognosis after infarction were evaluated in 686 patients with stable angina who were randomly assigned to medical or surgical treatment in the Veterans Administration Cooperative Study of Coronary Artery Bypass Surgery. METHODS AND RESULTS: Myocardial infarction was defined by either new Q wave findings or clinical symptoms compatible with myocardial infarction accompanied by serum enzyme elevations with or without electrocardiographic findings. Treatment comparisons were made according to original treatment assignment; 35% of the medical cohort had bypass surgery during the 10-year follow-up period. The overall cumulative infarction rate was somewhat higher in patients assigned to surgery (36%) than in medical patients (31%) (p = 0.13) due to perioperative infarctions (13%) and an accelerated infarction rate after the fifth year of follow-up (average, 2.4%/yr in the surgical group versus 1.4%/yr in the medical group). The 10-year cumulative incidence of death or myocardial infarction was also higher in surgical (54%) than in medical (49%) patients (p = 0.20). According to the Cox model, the estimated risk of death after infarction was 59% lower in surgical than in medical patients (p less than 0.0001). The reduction in postinfarction mortality with surgery was most striking in the first month after the event: 99% in the first month (p less than 0.0001) and 49% subsequently (p less than 0.0001). The estimated risk of death in the absence of infarction was nearly identical regardless of treatment (p = 0.75). Exclusion of perioperative infarctions did not alter the findings. CONCLUSIONS: Although surgery does not reduce the incidence of myocardial infarction overall, it does reduce the risk of mortality after infarction, particularly in the first 30 days after the event (fatal infarctions).

Angina Pectoris↗

PubMed1997

Safety and accuracy of dobutamine-atropine stress echocardiography for the detection of residual stenosis of the infarct-related artery and multivessel disease during the first week after acute myocardial infarction.

BACKGROUND: The safety of dobutamine-atropine echocardiography early after acute myocardial infarction is unknown. Its accuracy for the early detection of infarct artery stenosis and multivessel coronary artery disease is also unclear. The objective of the present study was to document its safety and accuracy during the first week after acute myocardial infarction. METHODS AND RESULTS: Multistage dobutamine-atropine stress echocardiography was performed in 232 patients (age, 58 +/- 13 years; 58 women) at 5 +/- 2 days after acute myocardial infarction. The peak heart rate was 116 +/- 20 bpm. There were no episodes of sustained ventricular tachycardia, myocardial infarction, or death. Atropine with dobutamine was tolerated well. Coronary angiography was performed in 206 patients (89%). There were 171 patients (83%) with infarct artery stenosis of > or = 50% and 114 patients (55%) with multivessel disease. Ischemic or biphasic responses in the infarction zone were 82% (140 of 171) sensitive and 80% (28 of 35) specific for residual stenosis. Sensitivity was similar for occluded arteries (77%, 36 of 47) and patent but stenotic arteries (84%, 104 of 124). Wall motion abnormalities outside the infarction zone were specific (97%, 89 of 92) and moderately sensitive (68%, 77 of 114) for multivessel disease. The only determinant of sensitivity for residual infarct artery stenosis was improved wall motion at low dose (P < .01). The determinants of sensitivity for multivessel disease were peak heart rate and infarct size (P < .01). CONCLUSIONS: Dobutamine-atropine stress echocardiography was safely used to detect residual infarct artery stenosis and multivessel disease during the first week after acute myocardial infarction. The test may be very effective for evaluating patients with acute myocardial infarction because sensitivity for residual stenosis and multivessel disease was maximal in the high-risk subsets of patients with viable, jeopardized myocardium and large infarct size.

Aged↗

PubMed2002

Decreased expression of Na+/H+ exchanger isoform 1 (NHE1) in non-infarcted myocardium after acute myocardial infarction.

Although cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in non-infarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury.

Animals↗

PubMedDate not supplied

Overestimation of myocardial infarct size on two-dimensional echocardiograms due to remodelling of the infarct zone.

OBJECTIVE: To assess the effect of early regional diastolic shape distortion or bulging of infarct zones due to infarct expansion on estimates of regional left ventricular dysfunction and infarct size by two-dimensional echocardiographic imaging. DESIGN: Quantitative two-dimensional echocardiograms from patients with a first Q wave myocardial infarction and creatine kinase infarct size data, and normal subjects, were subjected to detailed analysis of regional left ventricular dysfunction and shape distortion in short-axis images by established methods. Regional left ventricular asynergy (akinesis and dyskinesis) and shape distortion indices (eg, peak [Pk]/radius [ri]) were measured on endocardial diastolic outlines of short-axis images in 43 postinfarction patients (28 anterior and 15 inferior, 5.9 h after onset) and 11 normal subjects (controls). In the infarction group, endocardial surface area of asynergy was calculated by three-dimensional reconstruction of the images and infarct size from serial creatine kinase blood levels. MAIN RESULTS: Diastolic bulging of asynergic zones was found in all infarction patients. The regional shape distortion indices characterizing the area between the 'actual' bulging asynergic segment and the derived 'ideal' circular segment (excluding the bulge) on indexed sections were greater in infarct than control groups (Pk/ri 0.31 versus 0, P < 0.001) and greater in anterior than inferior infarction subgroups (Pk/ri 0.39 versus 0.16, P > 0.001). Importantly, the degree of distortion correlated with overestimation of asynergy (r = 0.89, P < 0.001), and the relation between infarct size and total 'ideal' asynergy showed a leftward shift from that with 'actual' asynergy. CONCLUSIONS: Early regional diastolic bulging of the infarct zone results in overestimation of regional ventricular dysfunction, especially in patients with anterior infarction. This effect should be considered when assessing effects of therapy on infarct size, remodelling and dysfunction using tomographical imaging.

Adult↗

PubMed1995

[A comparison of risk factors between silent brain infarction and symptomatic brain infarction--clinical significance of hypertension and diabetes mellitus].

We studied a clinical significance of hypertension and diabetes mellitus between silent brain infarction and symptomatic brain infarction. History of hypertension was present in 50% of silent infarction and in 53.3% of symptomatic infarction. Untreated hypertension was more frequent in symptomatic infarction than silent infarction (28.3% vs 16.7%) and the control of the blood pressure was very poor even if the patients with symptomatic infarction was treated with antihypertensive drugs. 66.7% of silent infarction with hypertension was treated with antihypertensive therapy and the control of the blood pressure was also relatively good. In the population with silent infarction, good control of the blood pressure was important for the prevention of symptomatic infarction. Diabetes mellitus with long history was strongly related to symptomatic infarction as compared with silent infarction. The prevalence of both hypertension and diabetes mellitus was high in the population with symptomatic infarction as compared with silent infarction and control individual.

Adult↗

PubMed2002

[Relation of pentanucleotide repeat polymorphism of apolipoprotein (a) gene to plasma lipoprotein (a) level among Chinese patients with myocardial infarction and cerebral infarction].

OBJECTIVE: Investigate the distribution and characteristics of 5'pentanucleotide TTTTA repeat (PNTR) polymorphism of apolipoprotein (a) [apo (a)] gene among Chinese patients with myocardial infarction (MI) and cerebral infarction, and its relationship to plasma lipoprotein (a) [Lp (a)] level. METHODS: DNA was extracted from the peripheral blood of 438 patients with myocardial infarction (MI, documented angiographically) and 218 controls, and 809 patients with cerebral infarction (documented by CT) and 1 817 controls. Plasma Lp (a) level was measured by ELISA. PNTR polymorphism of apo (a) gene was determined by polymerase chain reaction (PCR) and subsequent polyacrylamide gel electrophoresis. RESULTS: Eight alleles and 29 genotypes in apo (a) PNTR were detected in the four groups. The frequency of (TTTTA)(4 - 7) allele in the cerebral infarction group was 7.0%, significantly higher than that in control group (5.4%, P < 0.05). The frequency of genotype (TTTTA)(5/8) in MI group was 13.2%, significantly higher than that in the control group (7.8%, P < 0.05). No significant difference was seen in other alleles and genotypes among different groups (all P > 0.05). The level of triglyceride (TG) in patients with MI was 5.13 mmol/L +/- 1.15 mmol/L, significantly higher than that in controls (4.90 mmol/L +/- 0.99 mmol/L, P < 0.05). The level of TG in patients with cerebral infarction was 1.84 mmol/L +/- 1.36 mmol/L, not significantly different from that in controls (1.83 mmol/L +/- 1.51 mmol/L). The level of total cholesterol (TC) in patients with MI was 4.85 mmol/L +/- 1.04 mmol/L, significantly lower than that in controls (4.97 mmol/L +/- 1.00 mmol/L, P < 0.001). The level of TC in patients with cerebral infarction was 1.97 +/- 1.11 mmol/L, not significantly different from that in controls (1.79 mmol/L +/- 1.23 mmol/L). A negative correlation between the number of PNTR and Lp (a) level was observed in both MI group (P < 0.001) and cerebral infarction group (P < 0.01), and not in the control group. Small fragment repeat of apo (a) PNTR was correlated with cerebral infarction (OR = 1.4, 95% CI: 1.040 approximately 1.910), not significantly with MI (P > 0.05). Multiple logistic regression analysis showed that individuals with plasma Lp (a) > 300 mg/L had higher risk of MI (OR = 2.4, 95% CI: 1.630 - 3.594), and a higher risk of cerebral infarction (OR = 1.6, 95% CI: 1.013 - 2.021) after adjustment for age, sex, SBP, DBP, BMI, smoking, TC, TG, HDL-C, LDL-C and Glu. CONCLUSION: Plasma Lp (a) is an independent risk factor for MI and cerebral infarction. PNTR of apo (a) gene was negatively correlated with Lp (a) levels both in MI group and cerebral infarction group. Association with PNTR genotype was only found in cerebral infarction, but not in MI.

Adult↗