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PubMed1997

Association of angiotensin I-converting enzyme gene polymorphism with myocardial ischemia and patency of infarct-related artery in patients with acute myocardial infarction.

OBJECTIVES: We determined the influence of angiotensin I-converting enzyme (ACE) insertion (I)/deletion (D) polymorphism on the extent of myocardial ischemia in patients with acute myocardial infarction. BACKGROUND: The I/D polymorphism, which in part controls plasma and tissue expression of ACE, has been implicated in predisposition to myocardial infarction and ventricular remodeling. METHODS: I/D genotyping, predischarge adenosine-thallium-201 perfusion tomography and radionuclide angiography were performed in 113 patients (72 men, 41 women) with a diagnosis of acute myocardial infarction. A subgroup of 96 patients also underwent coronary angiography. RESULTS: Genotypes DD, ID and II were present in 27, 56 and 30 patients, respectively. There was no significant difference in the baseline characteristics of patients, total creatine kinase, peak MB fraction, Killip class, mean ejection fraction or the number of diseased vessels in patients with the DD, ID or II genotype. However, the size of the total and the reversible perfusion defects was greater in those with DD than in those with ID or II genotype (total defect size [mean +/- SD] 33.7 +/- 22.5%, 29.5 +/- 19.2% and 22.2 +/- 16.0%, respectively [p = 0.022]; reversible defect size 18.0 +/- 16.0%, 12.1 +/- 11.6% and 8.2 +/- 7.8%, respectively [p = 0.006]). Occlusion of the infarct-related artery was also more common in patients with DD genotype (odds ratio 3.9, 95% confidence interval 1.4 to 11.0). Multivariate analysis showed that the I/D genotype was an independent predictor of perfusion defect size and patency of the infarct-related artery (p = 0.001). CONCLUSIONS: DD genotype was associated with a larger ischemic defect and occlusion of the infarct-related artery. Patients with DD genotype, having a larger ischemic defect, are expected to be at a greater risk for subsequent cardiovascular events.

Adenosine↗
PubMed1998

The Association of Anticoagulant Protein Concentrations with Acute Myocardial Infarction in the Thromholysis in Myocardial Infarction Phase II (TIMI II) Trial.

Background: Little is known about the relationship between myocardial infarction and the coagulation inhibitors protein C, protein S, and antithrombin III (ATIII). Methods: We explored the hypothesis. that partial deficiencies in protein C, protein S, and ATIII may be associated with acute myocardial infarction by comparing the baseline levels of these anti coagulants in a sample of participants in the Thrombolysis in Myocardial Infarction Phase II Trial (TIMI II) to the levels in a sample of Red Cross donors. We also examined the changes in concentrations of hemostatic and inhibitory factors during thrombolytic therapy, the correlations between the inhibitors and plasminogen and fibrinogen, and the association of baseline inhibitor levels with the degree of plasmin generation during treatment. Levels of protein C, free and total protein S, ATIII, fibrinogen, tissue-type plasminogen activator, (t-PA), plasminogen, and alpha-2 antiplasmin were measured in plasma samples obtained at baseline before treatment with thrombolytic therapy and at 50 minutes, 5 hours, and 8 hours after the start of therapy (n=92). Protein C, free and total protein S, and ATIII were also measured in plasma samples from comparable Red Cross donors (n=92). Results: Baseline protein C and ATIII levels were higher in the TIMI II subjects than in controls (3.7 µ/ml vs 3.3 for protein C, P=0.002; 118% vs 111% for ATIII, P=0.006). Free and total protein S levels were lower in the TIMI II subjects than in controls (4.3 µ/ml vs 5.2 for free protein S, and 15.3 µ/ml vs 17.2 for total protein S, P=0.001). There were no major changes in protein C or protein S levels after initiation of thrombolytic therapy, but there was a 13% decrease in ATIII. Significant correlations were found between baseline protein C, Protein S, ATIII, and plasminogen; none of these factors were correlated with baseline fibrinogen concentration. The pretreatment levels of the inhibitors were correlated with markers of the amount of plasmin generated during therapy. Conclusions: It is not likely that partial protein C or ATIII deficiency is commonly associated with myocardial infarction. It is more likely that at the time of infarction, these inhibitors are somewhat higher possibly due to a homeostatic response to previous plaque rupture and thrombosis. Partial protein S deficiency may play a role in coronary thrombosis. The levels of these inhibitors at the time of infarction may be important in the efficacy of thrombolytic therapy.

Journal Article↗
PubMedDate not supplied

Experimental cerebral infarction. Part 1: Production of thalamic infarction in dogs.

Difficulties in achieving focal temporary cerebral ischemia in experimental animals have delayed study of the prevention and treatment of cerebral infarction. We have succeeded in producing focal cerebral infarction by temporary occlusion of brain arteries. Infarction confined to the anterior portion of the thalamus was obtained by simultaneous occlusion of the 4 cerebral arteries: internal carotid, anterior cerebral, middle cerebral and posterior communicating arteries for 60-120 minutes. This experimental model in dogs is unique, since thalamic infarction can be produced with high frequency, and the dogs can be kept alive and managed for sufficient periods after temporary artery clipping. With this model it is possible to investigate cerebral infarction not only from the pathophysiological viewpoint, but also from the viewpoint of prevention and treatment of cerebral infarction in man.

Animals↗
PubMed1978

[Experimental cerebral infarction. Part 2: EEG change in experimental thalamus infarction in the dog--it's value and application (author's transl)].

Athough it has been generally believed that it is extremely difficult to prepare an experimental model of cerebral infarction in the dog with the use of temporary vascular occlusion, the procedure recently developed by one of the authors fascilitates the production of a localized infarction in the thalamus with a noticeably high rate of success. To obtain more reliability of this method, techniques of electroencephalography induced from depth electrode to the thalamus were applied in this experiment. Following a temporary vascular occlusion, a significant diminution of fast wave component of about 10 Hz occurred with attenuation of voltage in the ipsilateral thalamic depth electrode. In cases of 2 hour vascular occlusion done by this method, an obvious infarction in the thalamus was confirmed histologically 7 days later. The authors emphasised that when the experimental model of thalamic infarction in the dog are combined with EEG, not only can cerebral infarction be producted with more certainly but also the EEG changes can be followed. This analysis is important since it provides information on the chronological changes in the ischemic region or infarction lesion.

Animals↗
PubMed2006

Combination of electrocardiographic and angiographic markers of reperfusion in the prediction of infarct size in patients with ST-segment elevation myocardial infarction undergoing successful primary angioplasty.

BACKGROUND: Optimal epicardial recanalization does not guarantee optimal myocardial perfusion. The aim of the current study was to evaluate angiographic and electrocardiographic markers of reperfusion in the prediction of infarct size in patients with STEMI undergoing successful primary angioplasty. METHODS: Our population is represented by 270 STEMI patients with ST successful primary angioplasty (postprocedural TIMI 3 flow and residual stenosis <50%) with available corrected TIMI frame count (cTFC), myocardial blush grade (MBG), ST-segment resolution and enzymatic infarct size (peak CK-MB) analyses. RESULTS: A significant linear relationship with enzymatic infarct size was observed for all markers of reperfusion, except for ST-segment resolution. These data were confirmed even when analyzed as continuous variables in case of cTFC (r=0.13, p=0.035), postprocedural residual cumulative ST-segment elevation (r=0.41, p<0.0001) and deviation (r=0.45, p<0.0001). At multivariate analysis applied to postprocedural angiographic and electrocardiographic markers of reperfusion, cumulative residual ST-segment deviation, myocardial blush grade, and corrected TIMI frame count were independent predictors of enzymatic infarct size. CONCLUSIONS: This study showed that, among patients with STEMI treated by primary angioplasty, cTFC, MBG and cumulative residual ST-segment deviation are independent predictors of infarct size. Therefore, angiography and electrocardiography may provide complementary information in the evaluation of myocardial perfusion.

Aged↗
PubMed2003

Influence of an antidiabetic treatment with sulfonylurea drugs on long-term survival after acute myocardial infarction in patients with type 2 diabetes. The LAngendreer Myocardial infarction and Blood glucose in Diabetic patients Assessment (LAMBDA).

INTRODUCTION: Patients with type 2 diabetes show a significantly higher mortality after acute myocardial infarction than non-diabetic patients. The influence of sulfonylureas on the survival after acute myocardial infarction is still under debate. PATIENTS AND METHODS: Survival of 562 patients, consecutively admitted to an intensive care unit with the diagnosis acute myocardial infarction, was prospectively assessed for > 3 years. At the time of hospital admission, patients were grouped as (a) non-diabetic patients; (b) patients with newly diagnosed type 2 diabetes; (c) patients with known type 2 diabetes not treated with sulfonylureas and (d) patients with known type 2 diabetes treated with sulfonylureas. Survival-analysis was performed according to Kaplan-Meier. RESULTS: 324 patients were non-diabetics, in 86 cases type 2 diabetes was newly diagnosed at the time of hospital admission, 77 patients with known diabetes had taken sulfonylureas (glibenclamide in all cases) prior to the acute myocardial infarction, 75 patients were on any other antidiabetic treatment. Long-term-survival was significantly shorter in patients with type 2 diabetes compared to the non-diabetic patients (p < 0.0001). However, no significant differences were observed between the patients with type 2 diabetes treated with sulfonylurea-drugs and those receiving any other antidiabetic treatment (p = 0.53) CONCLUSIONS: An antidiabetic treatment with sulfonylurea-drugs prior to acute myocardial infarction does not have negative effects on the long-term survival. Larger prospective studies will be necessary to finally clarify this question.

Acute Disease↗
PubMed2002

Reduction of new coronary events and new atherothrombotic brain infarction in older persons with diabetes mellitus, prior myocardial infarction, and serum low-density lipoprotein cholesterol >/=125 mg/dl treated with statins.

BACKGROUND: We report the incidence of new coronary events and new atherothrombotic brain infarction (ABI) in older men and women with diabetes mellitus, prior myocardial infarction, and a serum low-density lipoprotein (LDL) cholesterol of >/=125 mg/dl treated with statins and with no lipid-lowering drug. METHODS: The incidence of new coronary events and of new ABI was investigated in an observational prospective study of 529 diabetics, mean age 79 +/- 9 years, with prior myocardial infarction and a serum LDL cholesterol of >/=125 mg/dl treated with statins (279 persons or 53%) and no lipid-lowering drug (250 persons or 47%). Follow-up was 29 +/- 18 months. RESULTS: At follow-up, the stepwise Cox regression model showed that after controlling for other risk factors, the use of statins was associated with a 37% significant independent reduction in the incidence of new coronary events and with a 47% significant independent reduction in the incidence of new ABI. CONCLUSIONS: Use of statins was associated with a 37% significant, independent reduction in new coronary events and a 47% significant, independent reduction in new ABI in older men and women with diabetes mellitus, prior myocardial infarction, and a serum LDL cholesterol of >/=125 mg/dl. Elderly diabetics with prior myocardial infarction and increased serum LDL cholesterol should especially be treated with statins.

Aged↗
PubMed2006

Is 15 mm size criterion for lacunar infarction still valid? A study on strictly subcortical middle cerebral artery territory infarction using diffusion-weighted MRI.

BACKGROUND AND PURPOSE: The 'lacunar hypothesis' has been challenged, since small (diameter <15 mm) subcortical infarcts can be produced by middle cerebral artery disease (MCAD) or cardioembolism (CE), while a larger infarct can occur without evidence of MCAD or CE. We sought to assess whether the lacunar hypothesis based on size is still valid. METHODS: We studied 118 patients who were admitted within 72 h after stroke onset and had acute deep subcortical MCA territory infarcts detected by diffusion-weighted MRI, and who had undergone angiography (mostly MR angiography). Stroke mechanisms were arbitrarily categorized regardless of lesion size: (1) MCAD when there was a corresponding MCA lesion; (2) internal carotid artery disease (ICAD) when there was a significant (>50%) ipsilateral ICAD; (3) CE when there was emboligenic heart disease without MCAD or ICAD, and (4) small vessel disease (SVD) when there was neither CE nor MCAD. SVD was further divided into definite SVD (dSVD, longest diameter <15 mm) or probable SVD (pSVD, longest diameter > or =15 mm). RESULTS: Seventy-three patients (62%) had SVD, of which 38 (32%) had pSVD and 35 (30%) dSVD. Thirty-three patients (28%) had MCAD, five (4%) CE, and seven (6%) ICAD. The infarct diameter in MCAD was not larger than in SVD (p = 0.35), and there was no difference in clinical features or risk factors between MCAD and SVD, or between pSVD and dSVD. CE was distinguished from SVD by its larger size and cortical symptoms. CONCLUSIONS: There are no clinical and lesion-size differences between MCAD and SVD, suggesting that there seems to be no rationale for the 15 mm size criterion for lacunar or small-vessel infarction.

Adolescent↗
PubMed1998

Right ventricular infarction causes heterogeneous autonomic denervation of the viable peri-infarct area.

BACKGROUND: Because efferent autonomic pathways to the right ventricle (RV) differ from the efferent autonomic projections to the left ventricle (LV), we assessed the effects of RV infarction on this innervation. METHODS AND RESULTS: We measured the ventricular effective refractory period (ERP) shortening in response to bilateral ansae subclaviae stimulation and ERP lengthening induced by bilateral vagal stimulation as markers of autonomic innervation before and after RV myocardial infarction (RVMI) produced by coronary ligation (n=28 dogs) or intracoronary latex injection (n=18 dogs) into a marginal branch of the right coronary artery in open-chest anesthetized dogs. In each dog, ERPs measured in viable peri-infarct area at two RV outflow tract (RVOT) sites and two septal and four lateral sites at the RV free wall after RVMI showed reduced or absent ERP shortening during bilateral ansae subclaviae stimulation laterally, septally, and at RVOT sites 3 hours after RVMI. ERP shortening in response to infused norepinephrine was still present. Bilateral vagal stimulation during background norepinephrine infusion (0.10 to 0.25 microg/kg per minute) lengthened the ERP at all test sites before latex injection. After transmural RVMI, vagally induced ERP prolongation was attenuated or lost at lateral, septal, and RVOT test sites. CONCLUSIONS: RVMI causes sympathetic and vagal denervation at viable sites at the RVOT, lateral, and, to a lesser extent, septal sides of the viable peri-infarct area. Autonomic denervation in the RVOT might contribute to the development of ventricular tachyarrhythmias after the acute stage of myocardial infarction involving the RV.

Animals↗
PubMed2002

[Acute promyelocytic leukemia accompanied by retinoic acid syndrome with complications of acute myocardial infarction and cerebral infarction during treatment with all-trans retinoic acid].

A 71-year-old man visited our hospital complaining of fever and a bleeding tendency. The peripheral blood WBC count was 10,400/microliter with 90% promyelocytes. The bone marrow was hypercellular with 88% promyelocytes. Disseminated intravascular coagulation was recognized. The patient was diagnosed as having acute promyelocytic leukemia and was treated with daily oral administration of all-trans retionic acid (ATRA) (45 mg/m2/day) and cytarabine (160 mg/day, intravenous drip infusion for the initial five days). The ATRA treatment induced leukemic cells to undergo mature myeloid differentiation. On day 24 after the start of treatment, the WBC count rapidly increased and acute myocardial infarction appeared, with consciousness disturbance and bilateral Babinski reflex appearing three hours later. Magnetic resonance imaging showed a fresh lacunar infarction of the right lenticular nucleus, and serum levels of IL-6 and PAI-1 were found to be elevated at the onset of infarction. Since there was a possibility that the retinoic acid syndrome (RAS) might have helped bring about the infarctions, we stopped the ATRA treatment and started administration of methyl-prednisolone (500 mg/body/day for 3 days) and gabexate mesilate. The WBC count decreased immediately and the consciousness disturbance improved. In this case, ATRA treatment might have initiated the RAS and resulted in some endothelial damage, thus causing the infarctions.

Aged↗
PubMed1996

[Regional cerebral blood flow and periventricular hyperintensity in silent cerebral infarction--comparison with multi-infarct dementia].

In order to investigate relationship between regional cerebral blood flow (rCBF) and the white matter lesions on MRI in silent cerebral infarction, we quantitatively measured rCBF by 123I-IMP autoradiography method (IMP ARG method) and single photon emission tomography (SPECT) in 36 patients with silent cerebral infarction (SCI group), 22 patients with multi-infarct dementia (MID group), and 16 control subjects without periventricular hyperintensity (PVH) and lacunar infarction on MRI (CL group). Regions of interest (ROIs) on rCBF images were set in the frontal (F), temporal (T), parietal (P), occipital (O) cortex, and the cerebral white matter (W). The severity of PVH on MRI T2-weighted image was divided into four grades (grade 0-3). Our results: 1) Though the frequency of hypertension was significantly higher in SCI group and MID group compared with CL group, no significant difference was seen in the mean age among these three groups. 2) rCBF in the white matter and cerebral cortices except the occipital cortex in SCI group was significantly low compared with CL group (gamma CBFSCI/gamma CBFCL: W 0.87, F 0.87, P 0.88, O 0.92). 3) rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex, in MID group was significantly low compared with SCI group (gamma CBFMID/gamma CBFCL: W 0.69, F 0.71, T 0.74, P 0.75, O 0.81). 4) The mean grade of PVH in MID group was significantly higher that that in SCI group (SCI 1.1 vs MID 2.5). 5) The severity of PVH was significantly correlated with each rCBF in the white matter and cerebral cortices, especially in the white matter and frontal cortex. Our findings suggest that the quantitative measurement of rCBF by IMP ARG method is useful for the follow-up study in the patients with silent cerebral infarction as well as the evaluation of the severity of PVH on MRI.

Aged↗
PubMed2005

Metabolic penumbra of acute brain infarction: a correlation with infarct growth.

Volume expansion associated with brain infarction occurs in perfusion-diffusion mismatch of magnetic resonance imaging. We aimed at elucidating the metabolic impairment of this phenomenon with (15)O positron emission tomography and perfusion and diffusion magnetic resonance imaging. Eleven patients with acute unilateral embolic occlusion of the internal carotid or middle cerebral artery were studied within 6 hours of onset. Regional cerebral blood flow and cerebral metabolic rate of oxygen (CMRO(2)) were compared with those in the contralateral cerebral hemisphere. The relative apparent diffusion coefficient of water was estimated as a marker of cytotoxic edema. Relative cerebral blood flow and relative CMRO(2) in an evolving infarct (normal diffusion initially, but abnormal on day 3) were significantly (p < 0.05) less than those in the periinfarct area (normal diffusion initially and on day 3). The relative apparent diffusion coefficient between the evolving infarct and periinfarct showed no significant difference. These findings indicated that the initial 3-day volume expansion of an embolic brain infarction was associated with disturbed CMRD(2) but not with cytotoxic edema as early as 6 hours after onset. The "metabolic penumbra" defined as normal water diffusion with depressed CMRO(2) is a target to reduce the volume expansion of brain infarction.

Aged↗
PubMed2001

Late (> 48 hr) myocardial infarction after PTCA: clinical and angiographic characteristics of infarction related or not to the angioplasty site.

Since late myocardial infarctions after percutaneous coronary interventions have not been well characterized, we intended to evaluate the characteristics of myocardial infarctions occurring > 48 hr after balloon angioplasty of native coronary arteries or saphenous vein grafts. The Montreal Heart Institute database (1985-1996) was interrogated for all patients readmitted with a diagnosis of MI more than 48 hr after successful percutaneous transluminal coronary angioplasty (PTCA). We compared the clinical, procedural, and angiographic variables between MIs related or not to the index PTCA site. One hundred and ninety-three patients presented with late myocardial infarction (MI) following balloon angioplasty. The median time elapsed between PTCA and MI was 55 days compared to 968 days when MI was unrelated to the PTCA site. MIs related to the PTCA site were more likely non-Q-wave (76% vs. 35%, P = 0.0001) with less marked CK-MB rise. Angiography showed less complex lesions (63% vs. 90%, P = 0.001) and better thrombolysis in myocardial infarction (TIMI) grade flow (TIMI II to III, 66% vs. 56%, P = 0.01) when the culprit lesion was at the PTCA site. Independent predictors of MI at the PTCA site were vein graft dilation, female sex, and residual stenosis post-PTCA. Myocardial infarctions occurring late after PTCA have a distinct time course and present specific characteristics according to their relationship or not to the previously dilated site.

Adult↗
PubMed2002

Limitation of infarct size and ventricular remodeling in patients with completely reperfused anterior acute myocardial infarction--the potential role of ischemia time.

BACKGROUND: Experimental studies suggest that coronary reperfusion does not result in appreciable myocardial salvage beyond 3 to 4 h. HYPOTHESIS: The present study was undertaken to examine the potential role of ischemia time as a determinant of infarct size and cardiac function in humans. METHODS: Ninety patients (69 men, 21 women, aged 61 +/- 1 years) presented within 24 h of onset of a first anterior infarct had ST-segment elevation on electrocardiogram. All patients underwent coronary intervention within 24 h of onset of symptoms and obtained complete reperfusion of the infarct-related artery. RESULTS: Infarct size expressed as a percentage of the area at risk (IS/RA) and left ventricular end-diastolic volume (LVEDV) were significantly (p < 0.017) smaller and left ventricula rejection fraction (LVEF) assessed by left ventriculography (35 +/- 4 days) was significantly higher in patients treated within 4 h after onset (IS/RA:55 +/- 4%, LVEDV: 127 +/- 7 ml, LVEF: 62 +/- 2%) than in those treated 4 to 12 h (97 +/- 2%, 140 +/- 13 ml, 52 +/- 3%) and 12 to 24 h (93 +/- 2%,163 +/- 14 ml, 49 +/- 5%) after symptom onset. Left ventricular end-diastolic volume was significantly smaller in patients treated 4 to 12 h after onset than in those treated 12 to 24 h after onset. CONCLUSIONS: Patients with < 4 h of myocardial ischemia exhibited significant myocardial salvage and better left ventricular function and patients with 4 to 12 h of myocardial ischemia exhibited significantly smaller LVEDV than those with more prolonged ischemia, although there was no difference in final infarct size.

Cardiac Catheterization↗
PubMed1979

Initial experience with transluminal recanalization of the recently occluded infarct-related coronary artery in acute myocardial infarction -- comparison with conventionally treated patients.

In 7 patients, the recently occluded infarct-related vessel was recanalized by transluminal catheter techniques during acute myocardial infarction (Group A). 4 patients had single-vessel disease, 2 patients two-vessels disease and one, involvement of three vessels. Control angiography was performed in 6 patients, 8 days to 7 months later. Changes of coronary artery anatomy and left ventricular function were compared with a group of 9 conventionally treated patients, who were found to have occlusion of the infarct-related vessel in the acute stage (Group B). Five Group B patients had one-vessel disease, 3 patients two-vessel disease and 1 patient, involvement of all three vessels. In the chronic stage, all transluminally recanalized vessels were found to be patent in Group A. There was spontaneous recanalization of the infarct vessel in 4 of 9 Group B patients. In Group A, the length of the akinetic segment (AKS) decreased significantly (p less than 0.05) from 145.4 +/- 48.5 mm to 73.2 +/- 73.4 mm (mean +/- SD). Volume parameters did not change significantly. In Group B, length of the AKS did not change significantly, EDVI increased significantly from 81.1 +/- 19.8 to 106.8 +/- 4.6 ml/m2 (p less than 0.05); ESVI increased significantly from 41.7 +/- 13.7; ml/m2 to 66.8 +/- 37.9 ml/m2 (p less than 0.01). In the acute stage, length of the AKS and volume parameters did not differ significantly between the two groups. In the chronic stage, AKS was significantly shorter (A: 73.2 +/- 63.4 mm; 144.9 +/- 59 mm (p less than 0.0025) and EF was significantly higher (A: 54.6 +/- 11.6%; B: 40.9 +/- 14.5% (p less than 0.05) in Group A. Peak CPK was lower in Group A (A: 1009 +/- 827 U/l; B: 1324 +/- 655 U/l), but this difference did not achieve statistical significance. Results of this pilot study suggest that transluminal recanalization in the early phases of acute myocardial infarction might result in limitation of myocardial injury. However, further research will be needed to improve the technique and to test its results.

Adult↗
PubMed1984

Relationship between electrocardiographically estimated infarct size and clinical findings in anterior myocardial infarction.

In 292 patients with anterior myocardial infarction (MI) and no previous MI the electrocardiographically estimated infarct size was correlated with clinical findings during hospitalization and 3-month follow-up. Patients with ECG-defined transmural MI had a higher incidence of different types of complications, such as congestive heart failure (CHF), hypotension, pericarditis, and a longer duration of hospitalization than patients with nontransmural MI. In a subgroup including 182 patients of the total series, a precordial map containing 24 electrodes was used. The sum of R waves (sigma R), the sum of Q waves (sigma Q), the number of Q waves, and sigma R - sigma Q were calculated 4 days after arrival in hospital to estimate the size of infarction. There was generally a correlation between these ECG variables and different clinical findings, such as incidence of CHF, hypotension, pericarditis, and the duration of hospitalization. It is concluded that the ECG determined infarct size in anterior MI in a majority of patients correlates with the incidence of different types of complications in acute myocardial infarction. In the individual patient, however, the risk of developing complications cannot be predicted by ECG changes.

Adult↗
PubMed1995

Management of myocardial infarction patients with an occluded infarct-related artery: additional commentary.

The evidence is becoming stronger (but not conclusive) that restoration of flow in the infarct-related artery at a later date than is generally accepted might decrease mortality. The CORAMI report suggests a good outcome with rescue angioplasty, but, unfortunately, there was no control group. Since urgent rescue PTCA opened the infarct-related artery in the 29% of patients who remained occluded after thrombolysis, those cardiologists advocating emergency PTCA in all infarcting patients argue that 100% of occluded vessels can be opened with PTCA. I don't argue that fact but would point out that 71% of these same patients would have had unnecessary angioplasty since the occluded artery would have opened with thrombolytic therapy. The randomized trial performed by Ellis and colleagues was a difficult one because of physician bias. It took three years to complete at 20 sites, and in the presence of an occluded anterior descending coronary artery some investigators were reluctant to randomize all of their patients to conservative therapy. Obviously, a large trial would be appropriate to confirm Ellis and colleagues' observations but I doubt this will ever be done. Based on what is now known, I think it is worthwhile to consider rescue angioplasty in patients with a known occluded infarct-related artery. Unfortunately, that means performing coronary angiography almost immediately in all patients with infarcting myocardium in order to identify those with persistant occlusion.

Adrenergic beta-Antagonists↗
PubMed1995

Captopril in acute myocardial infarction: beneficial effects on infarct size and arrhythmias.

It is known from experiments that angiotensin-converting enzyme inhibitors can limit infarct size. In a prospective, randomized, placebo-controlled double-blind study, 22 patients were given 1.5-2.0 mg captopril/h i.v., while 24 patients were given placebo. Medication was started between 2 and 18 h from the onset of infarction. The two groups were matched for age, infarct location, and time of intervention. With the exception of one patient in either group, all were concurrently given nitroglycerin. The necrosis parameters were provided by the quantitative measurement of the QRS complex. The Q wave decreased with captopril treatment (-0.003 mV), but increased with placebo (+0.14 mV, p < 0.05). The number of ventricular premature beats at 24 h from the start of treatment was 25/h with placebo, and 9/h with captopril (p < 0.02). Ventricular fibrillation occurred seven times in the placebo group, but did not occur in the captopril group. The creatine kinase infarct weight was 59 gram-equivalents (gEq) with placebo, and 45 gEq with captopril (p = NS). Mean arterial pressure was reduced by 12 mmHg with captopril treatment. The results show a beneficial effect of captopril on infarct size and electrical instability, over and above the effect of standard management with nitroglycerin and thrombolysis.

Angiotensin-Converting Enzyme Inhibitors↗