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PubMed2005

Relationship between residual blood flow in the infarct-related artery and scintigraphic infarct size, myocardial salvage, and functional recovery in patients with acute myocardial infarction.

UNLABELLED: In patients with acute myocardial infarction (AMI) before primary coronary stenting with adjunct glycoprotein IIb/IIIa receptor blockade, whether residual blood flow in the infarct-related artery (IRA) affects infarct size or myocardial salvage is not known. METHODS: This study included 118 patients with ST-segment elevation AMI who received coronary stenting plus abciximab. SPECT studies were performed before and 7-14 d after stenting. RESULTS: Patients were divided into a group with initial Thrombolysis in Myocardial Infarction (TIMI) flow grade < or = 1 (77 patients) and a group with initial TIMI flow grade > 1 (41 patients). The initial median perfusion defect and (in brackets) the 25th and 75th percentiles were 29.1% [21.0%; 52.0%] of the left ventricle in patients with TIMI flow grade < or = 1, versus 16.5% [8.0%; 33.1%] of the left ventricle in patients with TIMI flow grade > 1 (P < 0.001). Baseline left ventricular ejection fraction (54.0% [45.0; 63.0] vs. 57.0% [40.0; 62.0], P = 0.623) or extension of hypokinetic region (28.0 [14.0; 41.0] hypokinetic chords vs. 24.0 [13.0; 39.0] hypokinetic chords, P = 0.643) did not differ significantly between the group with TIMI flow grade < or = 1 and the group with TIMI flow grade > 1. Final infarct size was 11.0% [6.1%; 23.5%] of the left ventricle in the group with TIMI flow grade < = 1, versus 6.0% [2.0%; 12.8%] of the left ventricle in the group with TIMI flow > 1 (P = 0.008). Salvage index was 0.58 [0.38; 0.76] in the group with TIMI flow grade < or = 1, versus 0.61 [0.36; 0.74] in the group with TIMI flow grade > 1 (P = 0.952). At the day 14 angiography, patients with TIMI flow grade > 1 had better left ventricular ejection fraction (61.0% [54.0%; 68.0%] vs. 56.5% [42.9%; 65.0%]; P = 0.03) and a smaller hypokinetic region (7 chords [0; 22.0] vs. 16 chords [2.5; 30.0]; P = 0.024) than did patients with TIMI flow grade < or = 1. CONCLUSION: Preserved blood flow in the IRA in patients with AMI is associated with a smaller area at risk, a smaller infarct, and better recovery of regional and global left ventricular function. The proportion of initial area at risk salvaged by coronary stenting does not seem to depend on residual blood flow in the IRA.

Aged↗
PubMed1998

Role of apoptosis in the disappearance of infiltrated and proliferated interstitial cells after myocardial infarction.

Myocardial infarction (MI) progresses from the acute death of myocytes and the infiltration of inflammatory cells into granulation, followed by scars. During the healing process, the myocardial interstitial cell population in the infarcted tissues increases markedly and then decreases. We postulated that apoptosis is responsible for this process. Twenty-four male Japanese white rabbits underwent a 30-minute occlusion of the left coronary artery followed by reperfusion for 2 days, 2 weeks, or 4 weeks (n=8 each). The histological features consisted of dead cardiomyocytes and marked leukocyte infiltration at 2 days after MI and granulation consisting of numerous alpha-smooth muscle actin-positive myofibroblasts, macrophage antigen-positive macrophages, and neovascularization at 2 weeks. At 4 weeks, the cellularity decreased markedly, and scars were evident. Interstitial cells with positive nick end labeling were significantly more frequent at the light microscopic level in the 2-day MI samples (5.3+/-3.6% in the center and 6.9+/-3.3% in the periphery of the infarct region) than in the 2-week (2.5+/-1.0%) and 4-week (0.5+/-0.5%) samples. DNA electrophoresis showed a clear ladder in tissues from the ischemic areas at 2 days after MI but not at 2 and 4 weeks after MI. Ultrastructurally, typical apoptotic figures, including apoptotic bodies and condensed nuclei without ruptured plasma membranes, were detected in leukocytes from all hearts with 2-day MI and in myofibroblasts, endothelial cells, and macrophages from all hearts with 2-week MI. In the electron microscopic in situ nick end labeling, immunogold particles intensely labeled the condensed chromatin of the typical apoptotic nuclei. These particles were also accumulated on nuclei of the interstitial cells showing homogeneous density but not definite condensation as typical apoptotic nuclei, suggesting an early stage of apoptosis. Thus, apoptosis plays an important role in the disappearance of both the infiltrated leukocytes and the proliferated interstitial cells after MI. This finding may have therapeutic implications for postinfarct ventricular remodeling through apoptosis handling during the healing stage of MI.

Animals↗
PubMed1989

Rehabilitation after a myocardial infarction.

Myocardial infarction is only one event in a chronic and progressive disease. A well-planned convalescence is part of the long-term promotion of a healthy and enjoyable lifestyle and provides the best possible prognosis.

Exercise↗
PubMed1998

Apoptosis and myocardial infarction.

Myocardial infarction was produced in rats and the contribution of apoptotic and necrotic myocyte cell death was measured quantitatively. Myocyte cell death by apoptosis involved 2.8 million cells at 2 hours after coronary artery occlusion and necrosis only 90,000 cells. Myocyte apoptosis continued to represent the major form of cell death, affecting 6.6 million cells at 4.5 hours, whereas myocyte necrosis peaked at 1 day, including 1.1 million cells. Apoptotic myocyte cell death was also present in the surviving portion of the wall adjacent to and remote from the infarcted myocardium where it peaked at 1-2 days. At this interval, 700/10(6) and 110/10(6) myocyte nuclei were undergoing apoptosis in the non-infarcted tissue bordering on and away from the ischemic area, respectively. Myocyte necrosis was absent in the viable myocardium after infarction. Since mechanical forces produced by pathologic loads may activate apoptosis, papillary muscles were exposed to high levels of resting tension in vitro and the magnitude of cell death in these samples was determined. Overstretching resulted in a 21-fold increase in apoptotic myocyte cell death which was coupled with the formation of reactive oxygen species, side-to-side slippage of myocytes, and depressed tension generation of the myocardium. In conclusion, apoptotic myocyte cell death plays a major role in ventricular remodeling after infarction, but whether physical forces, oxidant stress, architectural rearrangement of myocytes, and impaired force development of the myocardium in vivo are causaly related requires further investigation.

Animals↗
PubMed1995

[Evaluation of myocardial fatty acid metabolism in the area of fill-in after thallium reinjection in patients with prior myocardial infarction].

Myocardial fatty acid utilization in the area with thallium fill-in after reinjection was assessed using 123I-labeled 15-(p-iodophenyl)3R,S-methylpentadecanoic acid (BMIPP). We studied 22 patients with prior myocardial infarction that revealed persistent defects on standard exercise-redistribution thallium imaging. In each patient, exercise-redistribution-reinjection thallium imaging was performed. Within two weeks of the thallium study, resting BMIPP imaging was performed 20 min after injection of BMIPP (148 MBq). Following qualitative analysis of the obtained thallium and BMIPP images, quantitative analysis was performed on the basis of relative regional uptake. Of 199 myocardial segments that showed persistent defects on exercise-redistribution images, 73 segments showed apparent fill-in on the reinjection images (fill-in positive), and the remaining 126 segments did not (fill-in negative). When BMIPP images were compared with the corresponding thallium reinjection images, reduced BMIPP uptake compared with thallium were frequently observed in the area of fill-in positive segments (65 of 73 segments, 89%). Quantitative analysis also showed decrease in BMIPP activity compared to thallium activity in the area of fill-in (49.7 +/- 16.1 vs. 65.8 +/- 16.0%, p < 0.001). In contrast, only 24 of the 126 fill-in negative segments (19%) showed lower BMIPP uptake than thallium. These results suggest that impaired fatty acid utilization in the area of thallium new fill-in after reinjection already exists at resting condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Predictive value of 99m-Tc-Sn(II) methylene diphosphonate in the study of acute myocardial infarction].

Myocardial scintigraphy with 99mTc-Sn (II)-Methylenediphosphonate (MDP) was performed in 90 patients with proven acute myocardial infarction (AMI), and in 37 subjects with acute chest pain of a different etiology, during the first five days after the onset of their illness. The procedure was 82.2% sensitive, 86.5% specific, and 83.5 accurate for the diagnosis of AMI. Based on the usual clinical, electrocardiographic and biochemical criteria, the likelihood of AMI in this population was of 70.9% before the scintigraphic test. Application of Bayes' Theorem showed an increase in the likelihood of AMI, from 70.9% to 93.7%, when myocardial scintigraphy was positive, an incremental ruling-in-gain of 22.8%. A normal scintigraphy, on the other hand, reduced the likelihood of AMI, from 70.9% to 33.4%, an incremental ruling-out gain of 37.5%. It is concluded that myocardial scintigraphy with MDP is an important clinical procedure for the study of patients with acute chest pain: a positive test tends to confirm AMI, while a normal image, although it reduces the likelihood of this disease, is not particularly helpful in ruling it out.

Bayes Theorem↗
PubMed2004

AT1 receptor blockade for the prevention of cardiovascular events after myocardial infarction.

Myocardial infarction is associated with high morbidity and mortality. Multiple therapeutic modalities have been shown to be effective in reducing adverse postmyocardial infarction outcomes. The most prominent drugs that have been used in this group of patients are those that oppose the effects of the renin-angiotensin-aldosterone system. These drugs include beta-blockers, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers and aldosterone blockers. Following initial success with angiotensin-converting enzyme inhibitors in reducing mortality and cardiac remodeling in postmyocardial infarction patients, recent focus has been on adjunctive or alternative use of angiotensin II-receptor antagonists. Multiple large-scale, randomized trials have been conducted in order to compare angiotensin II-receptor antagonists with a combination of angiotensin II-receptor antagonists and angiotensin-converting enzyme inhibitors, and with angiotensin-converting enzyme inhibitors alone in postmyocardial infarction patients and also in heart failure. Although some results are conflicting, the weight of evidence is towards equivalency of these two groups of medicines, provided that the maximum effective dose of the angiotensin II-receptor antagonists is used. The combination of an angiotensin-converting enzyme inhibitor and an angiotensin II-receptor antagonist may have additional benefits for some, but not all, patients; for example, reducing morbidity and mortality in patients with chronic heart failure but not in postmyocardial infarction patients. Indeed, in the postmyocardial infarction setting, the combination appears simply to increase the side effects, without conferring additional benefits. Use of aldosterone antagonists as adjunctive therapy in postmyocardial infarction patients is associated with added benefits in terms of mortality reduction and will become the standard of care in this group of patients.

Adrenergic beta-Antagonists↗
PubMed1992

Myocardial uptake of antimyosin antibody compared with serum myosin light chain I levels in patients with myocardial infarction.

Myocardial accumulation of In-111-antimyosin (InAM) was evaluated in comparison with circulating serum myosin light chain I (LCI) level at the time of InAM injection. Seventeen consecutive patients were studied at various stages ranging from 6 days to 34 days after myocardial infarction (MI). The infarct area was positive for InAM uptake in all patients (100%), and significant myocardial uptake was observed in 14 patients (82.4%). The intensity of InAM uptake correlated with the infarct location shown by ECG and CAG. In contrast, 12 patients (70.6%) had normal or undetectable serum myosin LCI levels, with 5 being normal (0.42-2.5 ng/ml) and 7 undetectable (0.42 ng/ml or less). Only 5 patients (29.4%) had elevated serum myosin LCI levels at the time of InAM injection, and this elevation was slight, ranging from 3.4 to 4.5 ng/ml (mean: 3.75 ng/ml). Among patients with undetectable, normal, and elevated serum myosin LCI levels, there was no significant correlation between InAM uptake and the serum myosin LCI level. Thus, even after the serum myosin LCI level has decreased to normal, InAM can still bind to cardiac myosin in patients with MI, presumably until there is complete recovery from the hibernating myocardium due to ischemic damage.

Adult↗
PubMed2001

Use of contrast echocardiography in the diagnosis of subacute myocardial rupture after myocardial infarction.

Myocardial rupture is an uncommon and catastrophic complication after acute myocardial infarction. It can present in an acute form or in a subacute form, with slower hemorrhage and thrombus formation at the site of rupture. These patients can survive several hours or days before the diagnosis is confirmed and the myocardial ruptured repaired. Two-dimensional Doppler echocardiography is very useful in the diagnosis of this complication, but the number of false-positive diagnoses is high, even in the presence of a large amount of pericardial effusion. In these patients, administration of a contrast agent can be useful to demonstrate active bleeding into the pericardium. We report a case of subacute myocardial rupture for which contrast echocardiography was useful in demonstrating the presence of persistent hemorrhage into the pericardium. To reduce the number of false-positive diagnoses, contrast echocardiography should be considered in patients with possible subacute myocardial rupture.

Aged↗
PubMed2006

ST-deviation patterns in recurrent myocardial infarctions.

Myocardial infarction (MI) may be classified as ST-elevation MI (STEMI) or non-STEMI (NSTEMI). We used the term "recurrent MI" (RMI) to denote repeat MI episodes in a particular patient in which a different coronary site is responsible for each episode. We investigated whether the type of RMI is more likely to be of the same type as the index MI or whether patients may have the 2 types of MI at random. The analysis included 305 patients who had >or=2 MI episodes. Acute MIs were classified as STEMI or NSTEMI. We attempted to include only MIs of native vessels, without the presence of extracardiac conditions that intensify myocardial ischemia. Most patients (76%) had repeat episodes of the same MI type, i.e., STEMI or NSTEMI. Recurrent STEMI occurred in 44% of patients, recurrent NSTEMI in 32%, and STEMI and NSTEMI in 24%. Thus, most patients with RMI episodes will have STEMIs or NSTEMIs but not the 2 types, suggesting a predilection of some patients to repeat episodes of occlusive thrombi and others to repeat episodes of nonocclusive thrombi.

Aged↗
PubMed1976

[Morphologic indices the influence of selenium and vitamin E on the course of experimental myocardial infarct].

Myocardial infarction was induced in rats by ligating a coronary artery. During a week they received daily injections of 50 mg/kg of vitamin E intramuscularly or 30 mug/kg of sodium selenite subcutaneously, or else a combination of these preparations. The control animals received no injections. Stereometrically a statistically significant reduction of the infarcted zone was noted under the effect of selenium, this reduction being especially distinct during the ischaemic stage; the maturation of granulation tissue with an enhancement of the fibroblast reaction therein was accelerated. The muscle cells of the myocardium beyond the infarction zone displayed an increased activity of lactate dehydrogenase and a reduced activity of succinate dehydrogenase, intactness of the ultrastructure of the cell pattern, an enhancement of the signs of ultrastructural regeneration. Vitamin E potentiated the effect of selenium and executed itself a similar, but less distinct effect.

Animals↗
PubMed1992

Myocardial infarction.

Myocardial infarction (MI) during pregnancy occurs approximately once in 10,000 pregnancies. The normal cardiovascular alterations associated with pregnancy may make the diagnosis of MI difficult. Nursing care focuses on astute assessment skills, provision of adequate oxygenation, and prolongation of the healing phase to prepare for the stress of delivery. Nurses caring for patients experiencing MI during the perinatal period require advanced cognitive knowledge and clinical skills to facilitate optimal maternal and fetal outcome.

Adult↗
PubMed1992

Supervised versus unsupervised exercise training following myocardial infarction and myocardial revascularisation procedures.

Exercise training is an important component of rehabilitative care for patients following myocardial infarction or myocardial revascularisation procedures. Participation of the patient in supervised exercise training, however, is not always practical, and home exercise training may be a reasonable alternative for low-risk patients. The relatively routine predischarge exercise test, performed for risk stratification, can identify low-risk patients and guide their exercise prescription during the early weeks at home. Advantages of home exercise training include increased availability and convenience and lower cost. Comparable improvements in functional capacity have been documented to result from home exercise and supervised group programmes. Drawbacks, however, involved the limited ability to teach patients the necessary safety precautions for exercise, the lack of opportunity to teach and encourage modification of coronary risk-related behaviours and lifestyles, and the lack of peer support. Several techniques have been proposed to overcome some limitations of home exercise and to encourage long-term adherence to the exercise regimen. Among these are telephone interaction between patients and nurses or other health professionals, transtelephonic exercise ECG recording, and the use of home exercise training videocassette. Comparative studies of the safety, efficacy, and costs of these approaches are needed; and means must be devised to provide the nonexercise-related information and counselling available to coronary patients in a supervised exercise setting.

Electrocardiography, Ambulatory↗
PubMed2004

Molecular dynamics of the compensatory response to myocardial infarct.

Myocardial infarct via occlusion of the left anterior descending coronary in rats caused overriding depression in transcription, signal transduction, inflammation and extracellular matrix pathways in the infarct zone within 24 h. In contrast, remote zone gene expression was reciprocally activated during the immediate post-infarct period. Infarct zone signal transduction occurred primarily through TGFbeta1 induction while the remote zone exhibited elevated WNT, NOTCH, GPCR and transmembrane signaling. A minimal day 1 acute phase, inflammatory response was detected in the infarct zone while interleukins (IL1alpha, IL1beta, IL6, IL12alpha, IL18) and the TNFalpha superfamily were activated in the remote zone. Different cytochrome subsets were activated in each left ventricular region on day 1 while anti-oxidant genes were elevated only in the remote zone. The infarct zone exhibited mixed early transcription factor activation across all binding domains with a balance favoring constitutive gene activation and differentiation pathways as opposed to cell proliferation. In contrast, the remote zone exhibited activation of extensive developmental transcription factors involved in specification of cell phenotype, tissue-specific interactions and position-specific cell proliferation on day 1. The day 28 infarct zone response mirrored the day 1 remote zone response including activation of genes associated with matrix remodeling (metallothionein and metalloproteinase 9, 12, 23), as well as genes associated with cell proliferation and phenotype specification (MYC, EGR2, ATF3, HOXA1) recapitulating developmental histogenesis programs.

Animals↗
PubMedDate not supplied

The cardiac, obstetric, and anesthetic management of pregnancy complicated by acute myocardial infarction.

Myocardial infarction (MI) occurring during pregnancy is a rare but potentially lethal event for both mother and fetus, particularly when it occurs in the third trimester or peripartum period. The authors report two cases of MI occurring in the third trimester of pregnancy and review the literature. Management of the acute infarct and the medical, obstetric, and anesthetic considerations in such patients during labor and delivery are discussed. Successful use of percutaneous transluminal coronary angioplasty is described in a patient with evolving MI and ongoing pain. The preferred method of delivery in the pregnant MI patient is addressed, with emphasis on the need for individualization of care and coordination between the cardiac, obstetric, and anesthetic teams. Finally, the authors review the risks of subsequent pregnancy in this patient population.

Adult↗
PubMed1990

Changes in heart function and cardiac cell size in rats with chronic myocardial infarction.

Myocardial infarctions were induced in rats by ligation of the left anterior descending (LAD) coronary artery. After 4 weeks, parameters of left (LV) and right ventricular (RV) function and of peripheral circulation were measured in the intact, anesthetized animals. The morphology of the heart chambers was examined at the macroscopic and cell size level. In animals with slight reduction in LV function, LVEDP was elevated from 3.4 +/- 0.8 to 8.8 +/- 1.5 mmHg, LV stroke work was reduced by 14%, and dP/dtmax of both ventricles was depressed by 10% compared with sham-operated controls. Myocytes isolated from the LV and RV were elongated to some extent and had a greater cell volume, but there was no change in heart weight. These rats had infarctions that were small or medium in size. In rats with severe depression in left heart function, cardiac output, LVSP, LV stroke work, mean arterial pressure, and the LV weight/body weight ratio were markedly lower than in sham-operated controls. LVEDP was elevated up to 32 +/- 2 mmHg. These rats had large infarctions. RVSP, RV weight/body weight ratio, and the volume of myocytes isolated from the RV were doubled. RV stroke work was increased by 58%. Myocytes from the LV, RV and from the septum were elongated to about the same extent. The septum had developed a 23% hypertrophy. Histological examination of the lungs revealed marked thickening of the tunica medica of small pulmonary arteries with narrowing of the lumen. These changes are considered to represent the morphological basis for the increased pulmonary vascular resistance that was associated with RV pressure overload and hypertrophy.

Animals↗
PubMed1978

[Prevention of myocardial infarct?].

Myocardial infarction remains one of the leading causes of mortality and morbidity in spite of the medical and surgical therapy currently available. Only the prevention of coronary atherosclerosis seems likely to modify this situation. Epidemiological studies have established hypertension, hypercholesterolemia and cigarette smoking, among others, as risk factors. Based on these findings, it was hypothesized that control of these factors might diminish the risk. This hypothesis has been tested in man repeatedly over the past twenty years. Except as regards cigarette smoking, the results of the studies are ambiguous. Before advising the general public on measures of prevention, more data on the etiology of atherosclerosis are needed.

Arteriosclerosis↗