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At least 19 recordsLinked to original sources
PubMed1997

Opposite effects of the remodeling of infarcted and non-infarcted myocardium on left ventricular function early after infarction in humans. An echocardiographic study in patients examined before and after myocardial infarction.

OBJECTIVE: The purpose of this study was to evaluate infarction-related changes in the infarcted and the non-infarcted myocardium using a baseline assessment of ventricular function obtained prior to the infarction. BACKGROUND: Experimental studies have shown that both infarcted and non-infarcted myocardium contribute to the process of left ventricular dilatation soon after the infarction, but no data exist on the effect that the infarct has on the pre-infarct ventricular morphology in humans. METHODS AND RESULTS: 10 patients, out of 721 admitted to our coronary care unit with a first acute myocardial infarction over a 3-year period, had had an echocardiographic examination performed before (354 +/- 407 days) and after (10 +/- 9 days) the infarction which were adequate for quantitative evaluation. Ventricular volume (Simpson) and regional wall motion (Centerline method) were evaluated by biplane apical sections and the endocardial length of the infarct and the non-infarct segments, imaged in a cross-sectional view at the papillary muscle level, were measured. After the infarction end-diastolic and end-systolic ventricular volume increased (P = 0.0003 and P < 0.0001, respectively); diastolic and systolic infarct segment length increased (P = 0.011 and P = 0.0008, respectively), while non-infarct segment had only diastolic lengthening (P = 0.019), without systolic changes. The ejection fraction decreased after the infarction (P < 0.0001), in inverse relation to infarct size and in direct relation to diastolic non-infarct segment lengthening. In the five patients in whom there was a significant diastolic lengthening of non-infarct segment (larger than mean +/- 2 S.D. of the interobserver variability) the decrease in ejection fraction was less than in the patients without significant lengthening of this segment (P = 0.017), despite a similar echocardiographic infarct size index. CONCLUSION: Ventricular enlargement early after myocardial infarction is due to both infarct expansion and lengthening of non-infarct segment. However, while systolic stretching of the infarct segment is a deleterious process that accounts for the increase in end-systolic volume, diastolic non-infarct segment lengthening is the expression of a functional compensatory mechanism that counteracts the reduction of the ventricular pump function secondary to the infarction.

Aged↗
PubMed1988

The size of infarction as judged enzymatically in 1974 patients with acute myocardial infarction. Relation with symptomatology, infarct localization and type of infarction.

A common data base of six coronary care units containing personal and clinical data of 17462 patients was used to investigate the relation between clinical symptoms of patients with acute myocardial infarction and size of infarction. In 1974 of the 5110 patients, in whom a final diagnosis of infarction was made, size of infarction was determined according to serially measured levels of serum alpha-hydroxybutyrate dehydrogenase. The episode of infarction was the first in 1396 patients, was recurrent in 497, and undetermined in 81 patients. We calculated the size factor (defined as the mean size of infarction of patients with a particular symptom divided by the mean size of infarction of patients without that symptom) to evaluate the role of the size of infarction to manifestation of certain clinical symptoms. Bradycardia, shock and right-sided failure when noted on admission to the coronary care unit, had factors for size of infarction significantly greater than 1.0 (1.15, 1.79 and 1.30, respectively) in patients suffering an initial infarction, but not significantly different from 1.0 in patients with recurrent infarction. The occurrence of primary and secondary ventricular tachycardia and/or fibrillation, left heart failure (Killip class II-IV), symptomatic supraventricular tachycardia, high-degree atrioventricular blocks, ruptures and death in the coronary care unit was associated with factors significantly greater than 1.0 in those patients having both initial and recurrent infarctions. The size of infarction as judged enzymatically was significantly larger in patients with anterior than inferior and lateral infarction. The size of infarctions without Q waves was judged to be generally 35% smaller than infarctions producing Q waves. It is concluded that the size of infarction determines the occurrence of several symptoms and complications diagnosed at admission or during stay in the coronary care unit.

Adult↗
PubMed1991

Intracerebral hemorrhage, cerebral infarction, and subdural hematoma after acute myocardial infarction and thrombolytic therapy in the Thrombolysis in Myocardial Infarction Study. Thrombolysis in Myocardial Infarction, Phase II, pilot and clinical trial.

In the Thrombolysis in Myocardial Infarction, Phase II pilot and clinical trial, 908 patients [326 (35.9%) in the pilot study and 582 (64.0%) in the randomized study] were treated with 150 mg recombinant tissue-type plasminogen (rt-PA) activator in combination with heparin and aspirin, and 3,016 patients [64 (2.1%) in the pilot study and 2,952 (97.9%) in the randomized study] were treated with 100 mg rt-PA in combination with heparin and aspirin. Adverse neurological events occurred in 23 patients treated with 150 mg rt-PA (2.5%) [nine cerebral infarctions (1.0%), 12 intracerebral hemorrhages (1.3%), and two subdural hematomas (0.2%)] and in 33 patients treated with 100 mg rt-PA (1.1%) [20 cerebral infarctions (0.7%), 11 intracerebral hemorrhages (0.4%), and two subdural hematomas (0.1%)]. The difference in adverse neurological events observed comparing the two rt-PA regimens was primarily due to a higher frequency of intracerebral bleeding among patients treated with 150 mg rt-PA (1.3% versus 0.4%, p less than 0.01). Patients with recent (within 6 months) histories of stroke were not eligible for the study, and patients with any history of cerebrovascular disease were declared ineligible early in the study. The small number of patients (89, or 2.3%) with any history of neurological disease, intermittent cerebral ischemic attacks, or stroke who were enrolled before the stricter eligibility criteria were imposed or on the basis of incomplete baseline information experienced an increased frequency of intracerebral hemorrhage compared with patients without such histories (3.4% versus 0.5%). Mortality at 6 weeks after presentation among 23 patients who had intracerebral hemorrhage was 47.8%. Intracerebral hemorrhage is a severe but infrequent complication of rt-PA therapy for acute myocardial infarction. The combined frequency of intracerebral hemorrhage, subdural hematoma, and cerebral infarction after treatment with 100 mg rt-PA is comparable to that observed in other trials with thrombolytic agents in acute myocardial infarction.

Cerebral Hemorrhage↗
PubMed1990

[Intravenous treatment with streptokinase of acute myocardial infarction. II. Effect of patency of the artery supplying the infarction area on the infarction size and post-infarction impairement of left-ventricular function].

153 patients with a first acute myocardial infarction underwent the study. 90 of them received 1.000.000 units of streptokinase intravenously, followed by intravenous heparin administration for 5-7 days. The control group consisted of 63 remaining. In all patients serum CK-MB activity was determined every 4 hours for 72 hours: the infarct mass was calculated from the obtained curves. In 118 patients selective coronarography and left ventriculography was performed in the 2-nd or 3-rd week of hospitalisation. Left ventricular ejection fraction (E.F.) and dyssynergy index were calculated from ventriculographic data. Coronarography revealed a patent infarct-related artery in 76.7% of patients treated with streptokinase and in 44.4% of the control group (p less than 0.001). Among patients with a patent infarct-related artery an early peak of serum CK-MB activity (suggesting early recanalisation) occurred in 72.2% of streptokinase patients but in only 42.1% of the control group. Patients with a patent infarct-related artery had a significantly lower infarct mass (45 +/- 28 g vs 56 +/- 30 g), a lower left ventricular dyssynergy index (229 +/- 243 vs 348 +/- 247) and a significantly higher E.F. (63 +/- 12% vs 54 +/- 15%) compared with patients with an occluded artery.

Cardiomyopathy, Dilated↗
PubMed2000

Early invasive versus ischaemia-guided strategies in the management of non-Q wave myocardial infarction patients with and without prior myocardial infarction; results of Veterans Affairs Non-Q Wave Infarction Strategies in Hospital (VANQWISH) trial.

AIMS: To compare the role of early invasive vs conservative management strategies in treating patients with non-Q wave myocardial infarction with or without a prior myocardial infarction. BACKGROUND: In patients recovering from non-Q wave myocardial infarction, the prognosis among patients with a first non-Q wave myocardial infarction is significantly better than in patients with a prior myocardial infarction, yet physicians often adopt an early invasive strategy to treat patients with a first non-Q wave myocardial infarction. METHODS: Non-Q wave myocardial infarction patients enrolled in the VANQWISH trial with a history of prior myocardial infarction were compared to those with a first non-Q wave myocardial infarction, for the trial primary end-point of death or myocardial infarction at 1 and 12 months, as well as for the initial randomized treatment strategy. RESULTS: Of the 920 non-Q wave myocardial infarction patients, 396 had a history of prior myocardial infarction and 524 did not. Patients with a history of prior myocardial infarction were older and had a higher incidence of multiple high-risk baseline characteristics than those with a first non-Q wave myocardial infarction. Compared to the group with a first myocardial infarction, the prior myocardial infarction group suffered more events at both 1 month (11% vs 6%, P=0.007) and at 12 months (29% vs 16%, P<0.001). This difference in outcome remained significant even after adjusting for confounding variables (P<0.0001 at 12 months). Among the non-Q wave myocardial infarction patients with a prior myocardial infarction, the frequency of death or recurrent myocardial infarction was similar in both invasive and conservative groups during the first year of follow-up. Among the first non-Q wave myocardial infarction group, those assigned to the conservative strategy had significantly fewer events (3% vs 9%, P=0.009 at 1 month; 12% vs 20%, P=0.016 at 12 months) and mortality (1% vs 5%, P=0.012 at one month; 5% vs 11%, P=0.009 at 12 months) than those assigned to early invasive strategy. CONCLUSION: A history of prior myocardial infarction identifies a moderately high-risk subset of non-Q wave myocardial infarction patients who display similar long-term outcomes regardless of the strategy assignment; however, patients with a first non-Q wave myocardial infarction may fare better with a conservative or ischaemia-guided approach during the first post infarction year.

Aged↗
PubMed1996

[Effect of infarct size and site, patency of the infarct vessel and perfusion of vital myocardium on remodeling of the left ventricle--studies with cine-magnetic resonance tomography in the first 6 months following myocardial infarct].

BACKGROUND: Aim of the study was to evaluate the influence of infarct size and location and patency of the infarction and non-infarction vessels on left ventricular morphology and function in the first 6 months after myocardial infarction. METHODS: 61 patients (17 female, 44 male, 36-83 years) were examined with Cine Magnetic Resonance Imaging (CMRI) 1 and 26 weeks, and with coronary angiography 4 weeks after infarction. 32 patients had anterior, 29 patients posterior myocardial infarction. 15 patients had small infarcts (< 20 gm), 19 intermediate sized (20-40 gm) and 27 patients large infarcts (> 40 gm). CMRI was done in short axis of the left ventricle. Left ventricular enddiastolic and endsystolic volume indices (LVEDVI, LVESVI), ejection fraction (LVEF), muscle mass (VM) and motility (VMOT) of the vital myocardium, mass (IM) and area (IA) of the infarction zone, and volume-mass-ratio (VMR) of the left ventricle were determined on each examination. RESULTS: After 6 months large infarctions had 25% more LVEDVI, 41% more LVESVI, 20% less LVEF, 11% more VM, 13% less VMOT, 13% more IM, 47% more IA, and a 17% increased VMR compared to small infarcts. Anterior infarctions showed 11% more LVEDVI, 19% more LVESVI, 7% less LVEF, 4% more VM, the same VMOT, 5% more IM, 21% more IA, and 6% more VMR than posterior infarctions. If the infarction vessel was not perfused, after 6 months LVEDVI was 12% more, LVESVI 19% more, LVEF 7% smaller, VM 4% less, VMOT the same, IM 5% more, IA 17% more, and VMR 7% more increased than in the group with open infarction artery. When both non-infarction vessels were stenosed, LVEDVI rose 24% more, LVESVI 49% more, LVEF fell 25% more, VM rose 12% more, VMOT fell 26% more, and VMR rose 12% more than in patients with indisturbed perfusion of the vital myocardium. CONCLUSION: Perfusions of the vital myocardium and infarct size seem to be the most important factors for post infarction remodeling of the left ventricle. Infarct location and patency of the infarction vessel are of less influence.

Adult↗
PubMed1998

Angiographic characteristics of infarct-related and non-infarct-related stenoses in patients in whom stable angina progressed to acute myocardial infarction.

BACKGROUND: In patients with coronary artery disease, angiographic and postmortem studies have shown that coronary stenoses in infarct-related arteries often have complex morphology. It is not known whether in patients with multivessel disease stenosis morphology in non-infarct-related arteries is different from those of the infarct-related arteries. METHODS AND RESULTS: In 24 consecutive patients we examined the angiographic characteristics of both the infarct-related stenoses and non-infarct-related stenoses before and after spontaneous acute myocardial infarction, by visual inspection and computerized edge detection of coronary angiograms. Before myocardial infarction, the severity of the infarct-related stenoses was <50% in 14 patients and > or =50% in 10 patients (p=not significant) and of non-infarct-related stenoses was <50% in 16 and > or=50% in 13. A significantly greater proportion of infarct-related stenoses with severity > or =50% progressed to non-Q-wave than to Q-wave myocardial infarction (71% vs 50%, p < 0.05). Before myocardial infarction, the percentage of concentric, eccentric, and irregular infarct-related stenoses was 8%, 13%, and 50%, respectively, whereas in the non-infarct-related stenoses it was 62%, 17%, and 21%, respectively (p < 0.01). A similar proportion of irregular morphology progressed to Q-wave or non-Q-wave myocardial infarction. CONCLUSIONS: In patients with stable angina who had acute myocardial infarction develop, the infarct-related and non-infarct-related stenoses on average are similar in severity but different in morphology. Nonsevere stenoses more frequently progress to Q-wave than to non-Q-wave myocardial infarction.

Adult↗
PubMedDate not supplied

Differential expression of three types of nitric oxide synthase in both infarcted and non-infarcted left ventricles after myocardial infarction in the rat.

In the present report we investigated the differential expression of three types of nitric oxide synthase (NOS) in the left ventricle after myocardial infarction in rats. One, 3, 7, 14, 28 and 56 days (n=6-12 for each group) after ligation of a coronary artery, tissue samples were obtained from infarcted and non-infarcted tissues. The mRNA and protein levels of neuronal (n) NOS, endothelial (e) NOS and inducible (i) NOS were sequentially determined by semi-quantitative reverse transcription-polymerase chain reaction and Western blotting. Progressive left ventricular dilatation and gradual reduction in fractional shortening were confirmed by echocardiography. The expression levels of nNOS were significantly increased 1, 3 and 7 days post-infarct compared to those of sham-operated rats in both the infarcted (P<0.01) and non-infarcted regions (P<0.01). Immunohistochemical analysis showed that nNOS was localized in nerve fibers in the left ventricle and that the number of positive fibers after myocardial infarction had increased compared to that in sham-operated rats. With regard to eNOS, no significant changes in expression levels were detected between infarcted hearts and sham-operated controls. The level of iNOS expression peaked three days post-infarct and then decreased in the infarcted tissue, whereas it increased one day post-infarct, peaked at 14 and 28 days post-infarct and was still elevated in the chronic stage in the ventricular septum. iNOS immunoreactivity was detected in spared cardiomyocytes and macrophages in the infarcted region, and in cardiomyocytes in the ventricular septum. The expressions of three types of NOS were differentially regulated and iNOS produced in the non-infarcted region may contribute to the progression of heart failure after myocardial infarction in rats.

Animals↗
PubMed1993

Serum C-reactive protein and infarct size in myocardial infarct patients with a closed versus an open infarct-related coronary artery after thrombolytic therapy.

Serum C-reactive protein rises in acute myocardial infarction, correlating positively with infarct size if thrombolytic treatment is not given. This correlation disappears if thrombolytic treatment is given, although the serum C-reactive protein concentration is still associated with the clinical outcome of the patient. We studied the effect of early coronary recanalization induced by thrombolytic treatment alone or combined with coronary angioplasty on the infarct related rise in serum C-reactive protein concentration. The C-reactive protein response caused by the myocardial infarct was lower in patients with an open infarct-related coronary artery than in patients with a closed infarct-related coronary artery, or in control patients who did not receive thrombolytic therapy. In control patients we found the expected strong positive correlation between infarct size and serum C-reactive protein (r = 0.58; P < 0.001, n = 48), which was similar to that in patients with a closed infarct-related coronary artery (r = 0.62; P < 0.001, n = 17). In patients with an open infarct-related coronary artery the correlation between infarct size and serum C-reactive protein was much weaker (r = 30; P < 0.01, n = 91). Consequently infarct size explained approximately 35% of the variation in serum C-reactive protein values in the control patients and 36% in the patients with a closed infarct-related coronary artery, but only 9% of the variation in the patients with an open infarct-related artery. Ejection fraction correlated negatively with serum C-reactive protein in both control and recanalized patients. The association was again much stronger in the control patients.(ABSTRACT TRUNCATED AT 250 WORDS)

C-Reactive Protein↗
PubMed1988

Nifedipine in acute myocardial infarction: an assessment of left ventricular function, infarct size, and infarct expansion. A double blind, randomised, placebo controlled trial.

The influence of nifedipine on left ventricular ejection fraction, infarct size, and infarct expansion was studied in a prospective, double blind, randomised, placebo controlled trial in 132 patients with low risk acute myocardial infarction of less than 12 hours duration, defined by an initial left ventricular ejection fraction greater than 35% and clinical Killip class of less than or equal to II. Sixty four patients were assigned to nifedipine 120 mg/day and 68 to placebo. Treatment was started on average (SEM) 8.0 (0.2) hours after onset of pain and continued for six weeks. Gated blood pool scans, thallium scans, and cross sectional echocardiograms were performed before treatment and at 10 days. There were no significant differences between the two groups in age, sex, cardiac risk factors, or use of other medications. Mean (SEM) global left ventricular ejection fraction was not different before treatment (nifedipine group 53 (2%), placebo group 55 (2%) and did not differ at 10 days (nifedipine group 54 (2%), placebo group 52 (2%). There were also no differences in regional wall motion or regional ejection fractions. Thallium defects quantified by computer analysis were similar in both groups before treatment (nifedipine 7.8 (0.7), placebo 7.9 (0.7)) and at 10 days (nifedipine 5.3 (0.7) placebo 5.3 (0.7)). In the subgroup of patients with transmural infarction who had good quality echocardiograms and serial studies (n = 30), there was no difference in mean (SEM) baseline infarct segment lengths between the two groups (nifedipine 70 (4) mm, placebo 65 (4) mm); however, the nifedipine group demonstrated no significant change in infarct segment length between the initial and 10 day studies ( + 0.6 (3) mm) while there was a significant increase in the infarct segment length in the placebo group (+ 7.8 (4) mm). The infarct segment length increased by >/= 1 cm in seven (47%) placebo patients but in only one (7%) nifedipine patient. The nifedipine group had a significant initial 10% decrease in mean arterial pressure whereas there was no change in the in the placebo group; this blood pressure difference persisted for 10 days. Thus although the early administration of nifedipine has no detectable effect on clinical outcome and infarction size, it may reduce early infarct expansion via an afterload reduction mechanism in patients with transmural infarction. These initial results must be interpreted with caution and need to be confirmed in a larger trial.

Adult↗
PubMed1994

Quantification of infarct size by thallium-201 single-photon emission computed tomography using the unfolded map method. Comparison with QRS score and angiographic infarct size at 4 weeks after infarction.

A new technique of data processing, the unfolded map method, was used with thallium-201 single-photon emission computed tomography to quantify infarct size in 35 patients with single-vessel disease at 4 weeks after their first myocardial infarction (24 anterior and 11 inferior infarcts), and the results were compared with those obtained by electrocardiography and contrast left ventriculography. The myocardial borders and the infarcted region were defined using the threshold technique and a cutoff value of 55%. Count profile data for each short-axis slice were unfolded zonally into single planes with the same ratio, and their areas were calculated from the slice thickness and radius. Thus, the size of the unfolded map represented the actual left ventricular myocardial area Infarct size was quantitated from the ratio of pixels in the infarcted region to those in the whole map, and the ratio itself was used as the percent infarct size. Although a defect 1 cm in diameter (0.8 cm2) could not be detected in a phantom study, defects > or = 2 cm in diameter (> or = 3.1 cm2) could be measured satisfactorily. The infarct size and percent infarct size determined by the unfolded map method correlated well with the QRS score (r = 0.841 and r = 0.838), the percentage of abnormally contracting segments on left ventriculography (r = 0.835 and r = 0.877), and the ejection fraction (r = -0.835 and r = 0.856). These data indicate that the unfolded map method provides adequate quantification of infarct size, even in the chronic phase, without complicated data processing.

Adult↗
PubMed1998

Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and stenosis severity.

Because 24% to 30% of patent infarct-related arteries occlude in the year following thrombolytic therapy for acute myocardial infarction, angiographic factors including corrected Thrombolysis in Myocardial Infarction (TIMI) frame count which may predict abnormal infarct-artery flow, require definition. We examined changes in coronary flow and infarct-artery lesion severity by computerized quantitative angiography over 1 year in 154 patients with a patent infarct-related artery 4 weeks after myocardial infarction. These patients were randomized to receive either ongoing daily therapy of 50 mg aspirin and 400 mg dipyridamole, or placebo. All angiograms were interpreted blind in our core angiographic laboratory. Infarct-artery flow, assessed by corrected TIMI frame counts, was normal (< or = 27) in 46% and 45% of patients at 4 weeks and 1 year, respectively. At 4 weeks, patients with corrected TIMI frame counts < or = 27 had higher ejection fractions (60+/-11% vs 56+/-12%; p = 0.04) than those with corrected TIMI frame counts >27. On multivariate analysis, corrected TIMI frame count and stenosis severity were predictive of late abnormal infarct-artery flow (TIMI 0 to 2 flow, both p <0.01). Only stenosis severity at 4 weeks predicted reocclusion at 1 year (p <0.0001). Aspirin and dipyridamole had no effect on flow or reocclusion. Thus, corrected TIMI frame count and stenosis severity at 4 weeks was highly correlated with infarct-artery flow at 1 year.

Aged↗
PubMedDate not supplied

Cost-effectiveness of streptokinase for acute myocardial infarction: A combined meta-analysis and decision analysis of the effects of infarct location and of likelihood of infarction.

OBJECTIVE: To determine the effects of infarct location and of the likelihood of infarction on the cost-effectiveness of intravenous streptokinase (IVSK) for suspected acute myocardial infarction (AMI). DESIGN: A meta-analysis of short-term survival was combined with a simple decision tree to determine marginal cost-effectiveness ratios for different infarct locations and different likelihoods of AMI (pMI). SETTING: Six randomized trials comparing IVSK with conservative treatment. PATIENTS: 31,940 patients with onset of symptoms of AMI from four to 24 hours earlier and, with the exception of one trial, electrocardiographic abnormalities. Patients with contraindications to thrombolytic treatment such as uncontrolled hypertension were excluded. MAIN RESULTS: If AMI is certain, treatment with IVSK has marginal cost-effectiveness ratios for each additional life saved of $9,900, $56,600, and $28,400, respectively, for patients with anterior, inferior, and other locations of AMI. If pMI is 50% treatment with IVSK has marginal cost-effectiveness ratios for each additional life saved of $22,700, $131,800, and $63,100, respectively, for patients with anterior, inferior, and other locations of AMI. CONCLUSIONS: The marginal cost-effectiveness ratio for IVSK therapy of inferior infarction is six times that for anterior infarction and rises steeply as the presence of AMI becomes less certain. Assuming society is willing to pay $250,000 per life saved, IVSK therapy should be given if the chance of acute anterior infarction exceeds 7%, if the chance of inferior infarction exceeds 32%, or if the chance of infarction in other locations exceeds 17%. In patients with suspected acute myocardial infarction, IVSK saves lives and is a reasonable use of societal resources.

Boston↗
PubMed1992

Early diagnosis of the site of infarction and the infarct-related coronary artery in patients with acute inferior myocardial infarction.

We evaluated the relationship between the site of infarction and the infarct-related coronary arteries from electrocardiograms (ECGs) recorded early after the onset of chest pain in patients with an initial acute inferior myocardial infarction (IMI). The subjects were 80 patients (mean age 57 +/- 12 years) with IMI admitted within 6 hours from the onset of chest pain. This was prior to the thrombolytic era. We analyzed the ECGs on admission, at 24 hours and at 4 weeks. All patients underwent left ventriculography and coronary angiography at 4-6 weeks from the onset of the IMI. Left ventricular ejection fraction (EF) and regional area changes were measured. The infarct-related coronary artery was determined by the site of the asynergy. Patients were allocated into 2 groups according to the infarct-related artery, i.e. right (RCA, n = 52) and left circumflex (LCX, n = 28). Parameters measured were ST elevation, amplitude and width of R wave and R/S ratio in leads V1 and V2, and amplitude of U waves in leads V1 to V3. We defined the U wave as a prominent positive U wave (PPU) if it was > 0.5 mm (50 microV) in height. A significantly greater number of patients with PPU showed asynergy in posterolateral segments compared to those without PPU. The EF was significantly lower in patients with PPU than in those without (46 +/- 12% vs 54 +/- 13%, p < 0.05). Patients with PPUs eventually showed ECG evidence of posterior infarction (increased R wave duration and R/S ratio > or = 1 in lead V1 or V2) by 4 weeks compared to those without PPUs. Also a significantly greater number of patients with PPUs developed posterior infarction shown by left ventriculograms than those without PPUs. As to the infarct-related coronary arteries, a significantly greater number of patients with LCX disease showed concomitant posterior infarction than those with RCA disease. Also, a significantly greater number of LCX patients showed PPUs and ST elevations in leads V5 and V6 than those with RCA disease. The sensitivity of PPUs and ST elevations in leads V5 and V6 suggesting LCX disease was 60% and the specificity was 98% with a predictive accuracy of 87%. Therefore, we conclude that PPUs in leads V1-3 and ST elevations in leads V5 and V6 are specific markers for the diagnosis of LCX-related infarction in the setting of evolving IMI.

Adult↗
PubMed1990

[Localization and type of acute myocardial infarct in relation to myocardial infarct size--patients with acute re-infarct].

A differentiated estimation of the acute re-infarction is individually necessary for the estimation of risk and prognosis. Thereby the methodical approach is of particular importance, since the further restriction of the remaining function of the myocardium in re-infarction is of fundamental significance. A monitoring for the establishment of CKmax as well as the measuring of the ejection fraction globally (EFg) allow a semiquantitative determination of the size of the myocardial infarction. This forms the basis for the evidence of smaller acute Q-wave re-infarctions and also of smaller acute re-infarctions of the posterior wall localization. The increase of the risk in non-Q-wave infarction (mean risk) and Q-wave infarction (high risk) in re-infarction could be confirmed by the ejection fraction globally. Thus significant differences of the surviving persons after acute re-infarction in comparisons to the primary infarction were elaborated.

Cardiac Output↗
PubMed1989

[Usefulness of coronary angioplasty (PTCA) of the infarct-related artery in patients with prior myocardial infarction--follow up of infarct zone pre- and post-angioplasty by stress thallium scan].

We studied the efficacy of coronary angioplasty (PTCA) of the infarct-related artery in 29 patients with prior myocardial infarction by stress thallium scan. Twenty-seven patients had anterior myocardial infarction (single LAD disease), one had inferior (single RCA disease) and one had posterior (single LCX disease). According to the stress-redistribution thallium scintigraphic finding before PTCA, the patients were classified in 4 groups; (A): three patients with complete redistribution. (B): fourteen patients with incomplete redistribution. (C): seven patients with partial redistribution. (D): five patients with no redistribution. After PTCA, the parameters of residual ischemia in the infarct area (% RD and Thallium ischemic score = TIS) were improved significantly but those of infarct size (RD% uptake and Defect Score = DS) were improved slightly in group A. In group B and C, % RD, TIS, RD% uptake and DS were all improved significantly. In group D, TIS was improved slightly and DS was improved slowly 3 months after PTCA. Group A had high probability of viable muscle and group D had high probability of scar at the infarct zone. Group B and C showed intermediate type between group A and D. The change of infarct area after PTCA was variable in 4 groups but both residual ischemia and infarct size decreased in all groups. Thus, PTCA of infarct-related coronary artery is useful even in the patients with prior myocardial infarction.

Adult↗
PubMed1984

Early dilation of the infarcted segment in acute transmural myocardial infarction: role of infarct expansion in acute left ventricular enlargement.

Left ventricular enlargement after myocardial infarction is a poor prognostic sign, the mechanism of which has not been well defined. Early left ventricular dilation may be due to the Frank-Starling effect, which results in an increase in the length of uninfarcted segments in response to a reduction in contractile muscle mass. In contrast to this adaptive physiologic mechanism, left ventricular dilation may alternatively be caused by a pathologic process that stretches and thins the infarcted myocardial segment (that is, infarct expansion). To determine the relative contributions of these two mechanisms to left ventricular dilation after an initial transmural anterior myocardial infarction, two-dimensional echocardiograms were obtained from 27 patients within 72 hours of the onset of symptoms of myocardial infarction and from 13 healthy control subjects. In the minor-axis echocardiographic view at the level of the papillary muscles, anterior and posterior endocardial segment lengths at end-diastole were measured with a microprocessor-based graphic system. The papillary muscles were used as internal landmarks to demarcate the anterior and posterior segments. Anterior (infarcted) segment length in patients with myocardial infarction was 11.6 +/- 2.2 cm (mean +/- SD), whereas in control subjects, anterior segment length was 8.6 +/- 1.2 cm (p less than 0.001). Posterior (uninfarcted) segment length in the patients was not significantly different from posterior segment length in the control subjects (5.4 +/- 1.2 versus 5.3 +/- 1.0 cm, respectively). Measurable left ventricular dilation during the first 3 days after transmural anterior myocardial infarction is due to dilation of the infarcted segment and not of the normal uninfarcted segment.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Selective inhibition of the contractile apparatus. A new approach to modification of infarct size, infarct composition, and infarct geometry during coronary artery occlusion and reperfusion.

BACKGROUND: Myocardial reperfusion is associated with calcium overload and cell contracture, mechanisms that may precipitate cell death. In this study, we tested the hypothesis that in vivo inhibition of this contracture could lead to cell preservation in an open-chest large animal model. METHODS AND RESULTS: Regional myocardium function was measured during a selective intracoronary infusion of 2,3-butanedione monoxime (BDM), a specific inhibitor of actin-myosin coupling, in the control state (10 pigs) and in a protocol of a 51-minute coronary occlusion followed by reperfusion (40 pigs). The effects on coronary artery blood flow in the basal state were also studied (seven pigs). Intramyocardial distribution of the infusate during coronary occlusion, myocardial water content after 30 minutes of reperfusion and area at risk, infarct size, type of histological necrosis, and infarct geometry after 24 hours of reperfusion were assessed. Methods used included electromagnetic flowmeter, radiolabeled microspheres, subendocardial sonomicrometers, fluorescein, triphenyl tetrazolium chloride and Masson's trichrome staining, and computer quantification of infarct edges. In the absence of ischemia, BDM infusion inhibited regional shortening in a dose-dependent manner up to full systolic bulging while producing marked regional increase in coronary blood flow. During early reperfusion, BDM reduced end-diastolic length 76% more than the control infusion (p less than 0.05) and increased systolic bulging by 420% compared with no change in control animals. The ratio of infarct size/area at risk was reduced by 31% with BDM (p less than 0.05), with striking modifications of infarct histology and infarct geometry; specifically, the extent of contraction band necrosis was reduced by 63% from 105.5 +/- 18.2 to 39.2 +/- 13.6 mm2 (p less than 0.02), and more patches of necrosis (6.5 +/- 2.1 versus 1.6 +/- 0.4, p less than 0.05) and higher contour (7.7 +/- 1.2 versus 5.03 +/- 0.2, p less than 0.05) and fractal (12.1 +/- 1.3 versus 7.8 +/- 0.2, p less than 0.05) indexes were found. CONCLUSIONS: Selective intracoronary infusion of BDM at doses inhibiting regional wall motion decreased infarct size after reperfusion. The effects of BDM on regional function, the reduction in contraction band necrosis at histology, and the peculiar configuration of these infarcts all suggest that inhibition of contracture can interfere with cell-to-cell progression of myocardial necrosis, supporting a role for contracture in reperfusion-induced cell death.

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