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PubMed1993

[The effect of transcardiac galvanization on the function of the microcirculatory bed of the peri-infarct area in experimental myocardial infarct].

The model of experimental myocardial infarction in rats was used to study the effect of procedures of transcardiac galvanization (the current power 4 mA, duration 60 min) on the condition of the peri-infarction zone microcirculatory bed. The morphometric studies of the microcirculatory bed were performed using PAS reaction with amylase using a net with equidistant points. Two runs of transcardiac galvanization by the end of the first 24 hours of myocardial infarction was shown to improve the condition of the capillary network, to increase the relative and absolute area of the capillaries, the number of opened reserve capillaries, to reduce the distance of oxygen and metabolites diffusion from capillaries to cardiomyocytes in the peri-infarction zone thereby creating favourable conditions for the remaining viable myocardium and for stabilization of the affected zone.

Animals↗
PubMed1993

Rapid infarct imaging with a technetium-99m-labeled antimyosin recombinant single-chain Fv: evaluation in a canine model of acute myocardial infarction.

Studies of monoclonal antibody-based imaging agents show that blood clearance is inversely proportional to molecular size, i.e., Fab or Fab' > F(ab')2 > IgG. Indium-111-antimyosin Fab-DTPA is a highly specific and sensitive marker for myocardial necrosis. An improvement on current antibody diagnostic imaging may result from the use of smaller labeled fragments. We report the first in vivo targeting of acute myocardial infarction with a novel recombinant single-chain Fv (sFv) antimyosin protein. The sFv (MW = 27,594) is approximately one-half the size of the Fab and is comprised of the heavy and light chain variable regions from the myosin-specific murine monoclonal antibody R11D10 which were joined by a 15-amino-acid linker and expressed as a fusion protein (sFv) in E. coli. The binding affinity of the sFv for cardiac myosin was similar to the affinity observed for the Fab fragment. Technetium-99m labeling of the sFv was accomplished by the attachment of a cleavable, ester-linked bifunctional chelator (RP-1). Comparative studies in mice showed 99mTc-sFv-RP-1 cleared significantly faster (p < 0.001) than 99mTc-Fab'-RP-1 and 111In-Fab-DTPA antimyosin fragments. Furthermore, measurement of 99mTc-sFv-RP-1 blood clearance in a canine model of acute myocardial infarction gave a mean T1/2 of 0.54 +/- 0.13 hr versus 2.80 +/- 0.57 and 2.58 +/- 0.64 hr for Fab-DTPA and Fab'-RP-1 (p < 0.05), respectively. Despite its comparatively rapid clearance, 99mTc sFv-RP-1 had similar uptake in the infarct compared to the Fab'-RP-1. In addition, infarct visualization was more rapid with the sFv. Thus, these data demonstrate antimyosin sFv possesses characteristics necessary for rapid imaging of myocardial necrosis.

Animals↗
PubMed1995

Reperfusion hastens appearance and extent of distribution of type I collagen in infarct zone: immunohistochemical study in rat experimental infarction.

BACKGROUND: The effects of reperfusion on time-dependent alteration of type I collagen have not been examined. OBJECTIVES: We compared the sequential changes in the appearance and distribution of type I collagen in reperfused infarct rat hearts to those in non-reperfused hearts. METHODS: Using an experimental rat model of infarction, we performed immunohistochemical staining with a polyclonal antibody to type I collagen by the avidin-biotin-peroxidase method. Reperfusion was established after 2-h coronary ligation that produced complete necrosis of myocytes. RESULTS: In reperfused hearts, type I collagen appeared in the peripheral zone of the infarct at day 2, which was 1 day earlier than in non-reperfused hearts. The extent of distribution of type I collagen in reperfused hearts was comparable to that observed approximately 1 day later in non-reperfused hearts. CONCLUSION: Reperfusion can accelerate collagen matrix formation compared with that in non-reperfused hearts after acute myocardial infarction.

Animals↗
PubMed1996

[Comparison of thrombolytic therapy and direct percutaneous transluminal coronary angioplasty for acute myocardial infarction: prospective multicenter trial at 16 clinical centers in Ibaraki prefecture TUGMI. Tsukuba University Group for Myocardial Infarction].

The efficacies of direct percutaneous transluminal coronary angioplasty (PTCA) and thrombolysis for the treatment of acute myocardial infarction were investigated in 80 patients treated within 12 hours of the onset of myocardial infarction by either PTCA (39 patients) or thrombolytic therapy (41 patients) followed by conservative care. The therapeutic approach was selected according to the treatment strategy at each of the 16 participating centers before the admission of the patients. The two treatment groups were closely matched in clinical characteristics except for the history of hypertension which occurred more in the thrombolysis group (22/39 vs 12/41, p = 0.026). The mean time before starting reperfusion therapy from the onset of symptoms was shorter in the thrombolysis group (2.3 +/- 1.5 vs 5.3 +/- 5.7 hours, p = 0.0001). Chest pain resolved more quickly in the PTCA group. Serial changes in the mean numbers of abnormal Q waves and mean values of the sum of elevated ST-segments on the electrocardiograms were similar in both groups. Serial changes of wall motion abnormality index on echocardiograms were similar in both groups. Coronary angiography after 4 weeks showed the thrombolysis group had greater residual luminal stenosis in the infarct-related artery. Left ventriculography after 4 weeks showed the PTCA group had better mean ejection fraction (68.1 +/- 11.2% vs 58.7 +/- 14.2%, p = 0.0263). Death (3/39 vs 1/41) and cardiac events (6/39 vs 6/41) after 4 weeks were similar in both groups. There was no significant difference in death and cardiac events between these two groups. However, the PTCA group had less severe residual luminal stenosis in the infarct-related artery and better left ventricular function after 4 weeks than the thrombolysis group.

Aged↗
PubMed1996

[Acute myocardial infarction in Chile: differences between men and women in its evolution and prognosis. Multicenter Study Group on Infarction] (GEMI)].

BACKGROUND: Gender may be a prognostic factor for the evolution of acute myocardial infarction and women may have higher mortality and complication rates. AIM: To study if there are differences in the evolution of acute myocardial infarction between men and women. PATIENT AND METHODS: We have recorded information on risk factors, clinical evolution, treatment and complications of 2,052 patients hospitalized for acute myocardial infarction in 36 Chilean hospitals. The odds ratio for female sex and mortality was calculated using a logistic regression analysis adjusted for risk factors, treatment, invasive procedures and complications. RESULTS: Twenty six percent of analyzed patients were female. Mortality rates among females and males were 11.8 and 20.2% respectively (p < 0.01). Women had higher frequency of smoking, diabetes, obesity and hypertension. Blood lipid levels were similar in both sexes. Compared to men, a lesser proportion of women were treated with thrombolytic agents (25 and 35% respectively), intravenous heparin (54 and 61% respectively), beta blockers (31 and 42% respectively) and intravenous nitrates (53 and 61% respectively). Also, women were subjected to less invasive procedures. The odds ratio for mortality and sex was 1.72 (confidence interval from 1.13 to 2.62). CONCLUSIONS: Female sex is an independent risk factor for acute myocardial infarction mortality.

Adult↗
PubMed1997

Effect of angiotensin-converting enzyme inhibition on infarct collagen deposition and remodelling during healing after transmural canine myocardial infarction.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibition for six weeks after myocardial infarction (MI) lowers the collagen content of infarct scars in dogs. However, temporal changes in collagen content of the infarct zone (IZ) with ACE inhibition during healing over six weeks after MI and their possible relation to IZ remodelling have not been determined. METHODS: IZ collagen (hydroxyproline) was measured over six to seven weeks in dogs treated with captopril (50 mg bid), enalapril (2.5 mg bid) or placebo, beginning on the second day following transmural anterior MI (or sham). In vivo changes in IZ and global left ventricular (LV) remodelling, mass and function (echocardiograms) and hemodynamics among six-week survivors were also measured. RESULTS: Compared with placebo, both inhibitors decreased IZ collagen (P < 0.001) over the seven weeks. Among the six-week survivors, both inhibitors lowered IZ collagen (P < or = 0.001) and increased the collagen type I:III ratio. However, preload was lower, increase in diastolic volume and mass were less and systolic function improved. Although the doses of captopril (but no enalapril) decreased afterload, inhibition of IZ collagen was less, IZ bulging and global LV dilation were less and systolic function was better with captopril than with enalapril. In all three MI groups, deaths over the seven weeks correlated with greater infarct size, LV volume and dysfunction and lower IZ collagen. CONCLUSIONS: ACE inhibition suppresses the temporal increase in IZ collagen and attenuates IZ expansion, thinning and bulging, and LV enlargement and aneurysm formation during healing after MI.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1977

[Hyperglycemia and the glucose tolerance test in the acute period of myocardial infarct and in the remote post-infarct period].

The blood sugar content was determined in 142 patients with myocardial infarction on the 1--3rd, 7-10th, 28--30th days of the disease by the Hagedorn-Jensen method. The standard glucose tolerance test was conducted in 64 patients on the 30th day of the disease and repeated in 20 patients 18 months after infarction. It was concluded that transient hyperglycemia developed in 47.8% of patients with myocardial infarction in the acute period, predominantly in those with a sugar curve of the diabetes-decipiens type. Carbohydrate tolerance was reduced in two thirds of the patients. In some of them this disorder was attended with clinical signs of diabetes and a severe course of myocardial infarction. In patients with diminished carbohydrate tolerance the sugar curve remained abnormal 18 months after the disease. Obvious diabetes developed in 6 out of 20 patients examined. Among relatives of patients with disturbed carbohydrate metabolism diabetes mellitus was encountered more frequently and the incidence of ischemic heart disease and hypertension was higher.

Acute Disease↗
PubMedDate not supplied

[Electrocardiographic data suggesting anteroseptal myocardial infarction, in presence of infarction of the left ventricle].

We present a case of right ventricular myocardial infarction, secondary to postangioplasty occlusion of ventricular ramus of the right coronary artery, that developed electrocardiographic changes suggestive of septal myocardial infarction, this diagnosis was eliminated through angiographic study. We conclude that the carefully analysis of the electrocardiographic changes in ST segment in V1 to V4 can guide to the diagnosis of right ventricular myocardial infarction. For that reason we recommend the routinary register of the right electrocardiographic derivations as V3R and V4R, and left derivations V7 and V8, that is, the thoracic circle, in all patients with acute myocardial infarction regardless its location.

Electrocardiography↗
PubMed2003

Frequency of subclinical lacunar infarcts in ischemic leukoaraiosis and cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy.

BACKGROUND AND PURPOSE: Small vessel cerebrovascular disease is an important cause of vascular cognitive impairment. It is usually sporadic but also occurs secondary to the genetic disorder cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). Recurrent lacunar stroke is a characteristic feature, although symptomatic events are relatively rare, making large numbers necessary for evaluation of potential therapies. Diffusion-weighted imaging is sensitive to acute ischemic lesions and differentiates them from chronic infarcts. Detection of asymptomatic lacunar infarcts with diffusion-weighted imaging is a potential surrogate marker for treatment trials. In this study, the frequency of asymptomatic new lesions in ischemic leukoaraiosis and CADASIL was determined as a step toward assessing the potential of this technique as a surrogate marker of disease activity. METHODS: Fifty patients with sporadic small vessel disease and 19 patients with CADASIL underwent diffusion-weighted imaging. All had been asymptomatic for 3 months before imaging. Diffusion-weighted images were screened by two raters for new lesions; lesions were confirmed as recent by a visible reduction of diffusivity on the corresponding apparent diffusion coefficient maps. RESULTS: Recent ischemic lesions were identified in four patients with sporadic small vessel disease (8.0%) and two patients with CADASIL (10.5%). CONCLUSION: Asymptomatic new lesions are found in cases of sporadic small vessel disease and CADASIL. The frequency of new lesions suggests that this approach has a potential role as a surrogate marker in therapeutic trials that warrants further investigation.

Adult↗
PubMed1997

Adjunctive Antiplatelet Therapy in Acute Myocardial Infarction: The Road to Improved Infarct-Related Artery Patency.

A direct relationship exists between infarct artery patency and survival in patients with acute myocardial infarction. Currently available thrombolytic regimens produce 90 minute patency rates on the order of 80%. Preliminary trials suggest that adjunctive anti-platelet therapy with glycoprotein IIb/IIIa inhibitors, in conjunction with thrombolytic therapy, may significantly improve 90 minute infarct related artery patency and thereby survival, in patients with acute myocardial infarction.

Journal Article↗
PubMedDate not supplied

Experimental cerebral infarction. Part 3: Protective effect of mannitol in thalamic infarction in dogs.

Whether or not mannitol can prevent infarctions in ischemic brain tissues was investigated utilizing the thalamic infarction model in dogs. Twenty dogs were divided into equal control and mannitol treatment groups. Temporary 4 vessel clipping for 60 minutes was adopted as the standard procedure for both groups. The only difference between the groups was the administration of 2 g/kg of mannitol before the arterial occlusion. In the controls, 6 of 10 dogs showed infarctions verified by histological changes at the seventh post-ischemic day. In the mannitol group only 1 dog in 10 showed infarction. The difference is statistically significant.

Animals↗
PubMed2005

Cyclophosphamide improves the function of post-infarct hearts by reducing old infarct area and accelerating the mobilization of CD34+ cells.

BACKGROUND: Myelosuppressives such as cyclophosphamide (Cy) and 5-fluorouracil (5FU), which can increase circulating CD34+ cells, may have a beneficial effect in the post-infarct heart. METHODS AND RESULTS: Twenty-four hours after 30-min ischemia-reperfusion, rabbits were intravenously treated with Cy (20 mg/kg), 5FU (15 mg/kg) or saline (S). Cy significantly improved cardiac function and remodeling and decreased the old infarct area 1 month after infarction, compared with those given S. The number of circulating CD34+ cells was higher and neovascularization and matrix metalloproteinase-1 was induced in the Cy group. CONCLUSION: Cy has potential for post-infarct treatment.

Animals↗
PubMed2005

Total flavones from Elsholtzia blanda reduce infarct size and improve heart function during acute myocardial infarction by inhibiting myocardial apoptosis in canines.

OBJECTIVE: The current study tests the hypothesis that inhibition of apoptotic cell death with total flavones from Elsholtzia blanda (TFEB), a traditional Chinese medicine, reduces infarct size and improves heart function during myocardial ischaemia induced by coronary occlusion in canines. METHODS AND RESULTS: Myocardial apoptosis was detected by the TdT-mediated dUTP nick end labelling (TUNEL) method and DNA laddering. Infarct size of the left ventricle, serum level of CK-MB, haemodynamic parameters including rate of rise and decline of left ventricular pressure (+/- dp/dtmax), left ventricular systolic pressure (LVSP), main arterial pressure (MAP), coronary blood flow (CBF), coronary vascular resistance (CVR) were measured in this study. TUNEL positive cells were markedly reduced from 27.83 +/- 8.15% in the control dogs to 7.74 +/- 3.50% in the TFEB-treated ones (P < 0.01), consistent with the absence of DNA laddering. TFEB significantly reduced infarct size from 19.30 +/- 6.66% in the control dogs to 8.87 +/- 1.66% (P < 0.01), confirmed by lower serum CK-MB activity. TFEB significantly reduced MAP and CVR. The decrease in +/- dp/dtmax, LVSP and CBF also tended to be much smaller in the TFEB treated group. CONCLUSION: These data suggest that the inhibitory effect of TFEB on apoptosis during coronary occlusion is associated with reduction in infarct size and improvement in heart function.

Animals↗
PubMed1978

[Experimental cerebral infarction.--Part 3: The protective effect of mannitol in thalamus infarction in dogs (author's transl)].

One day during an aneurysm surgery under the preoperative administration of mannitol, the feeding artery was accidentally occluded temporarily. Since then, investigation on whether or not mannitol can prevent infarctions in ischemic brain tissues have been carried out utilizing the thalamus infarction model in dogs. Twenty dogs were divided into equal groups, the control and the mannitol group. Temporary clipping for sixty minutes was adopted as a standard for both groups. The only difference between the groups was the administration of 2 g/kg of mannitol before the arterial occlusions. In the control, six of ten dogs showed infarctions verified as histological changes on the seventh post-ischemic day. In the mannitol group only one of ten showed infarction. Each of the difference is statistically significant (P less than 0.03).

Animals↗
PubMed1987

Role of infarct expansion in rupture of the ventricular septum after acute myocardial infarction: a two-dimensional echocardiographic study.

To verify the role of infarct expansion (IE) in ventricular septal rupture (VSR) after transmural acute myocardial infarction (TAMI), topographic parameters were measured using tomographic imaging with two-dimensional echocardiography (2-D echo) and computer-aided analysis in four groups of patients: 8 patients with VSR (Group 1); 24 patients with TAMI but no mechanical complications (Group 2); 11 normal athletes (Group 3); 5 adults with congenital ventricular septal defect (Group 4). Measurements made on end-diastolic outlines of mid-left ventricular (LV) short-axis images included: LV asynergy (akinesis and/or dyskinesis), expansion index (asynergy/nonasynergy-containing endocardial segment length), thinning ratio (asynergic/nonasynergic wall thickness), and new indexes of regional shape distortion (RSD) by quantifying the deviation of the actual asynergic segment from the ideal asynergic arc constructed using the nearly circular nonasynergic contour. In Group 1, clinical IE (hypotension, congestive heart failure, no signs of new infarction) preceded detection of the VSR and portable 2-D echo showed the VSR associated with LV asynergy, marked IE, and RSD. Although Groups 1 and 2 had similar LV asynergy (28.7 vs. 26.9% LV) and ejection fraction (38.9 vs. 41.8%), Group 1 had higher expansion index (1.50 vs. 1.17, p less than 0.05), lower thinning ratio (0.54 vs. 0.67, p less than 0.005), and higher RSD parameters (e.g., peak distortion, Pk or maximum radial distance from the ideal arc, 19.3 vs. 3.9 mm, p less than 0.01; area of distortion, Ad, 7.4 vs. 1.1 cm2, p less than 0.05) than Group 2. Groups 3 and 4 had normal regional and global function and no evidence of expansion, thinning, or RSD. Thus, IE with marked diastolic RSD on an early 2-D echo after TAMI might identify patients at risk for VSR.

Aged↗
PubMed1989

Ventricular septal and free wall rupture complicating acute myocardial infarction: experience in the Multicenter Investigation of Limitation of Infarct Size.

Left ventricular rupture was studied in 849 patients enrolled in the Multicenter Investigation of Limitation of Infarct Size. Although documented rupture occurred in only 14 cases (1.7%), it accounted for 14% of in-hospital mortality. Seven of the 14 ruptures occurred within 2 days and 10 within 4 days of the MB-creatine kinase-determined onset of infarction. Three easily determined baseline characteristics defined a set of patients with a markedly increased risk of myocardial rupture. Rupture was 9.2 times more likely to occur in patients with all of the following characteristics than in the remaining patients: (1) no history of previous angina or myocardial infarction, (2) ST segment elevation or signs of Q wave development on the initial ECG, and (3) peak MB-creatine kinase value (greater than or equal to 150 IU/L). The risk of myocardial rupture with these three characteristics was 5.5%. Although these predictors are likely to be of little therapeutic value for free wall rupture, since most patients with that complication die within minutes of its onset, they may aid in alerting physicians to the early diagnosis and timely surgical correction of ventricular septal rupture.

Creatine Kinase↗
PubMed1988

Rupture of the left ventricular free wall during acute myocardial infarction: analysis of 138 necropsy patients and comparison with 50 necropsy patients with acute myocardial infarction without rupture.

Clinical and necropsy findings in 138 patients (69 men and 69 women) with rupture of the left ventricular (LV) free wall during acute myocardial infarction (AMI) (rupture group) were compared with 50 patients who died during their first AMI without rupture (nonrupture group). The frequency of systemic hypertension (55 vs 52%), angina pectoris (13 vs 22%) and congestive heart failure (0 vs 0%) before the fatal AMI was similar for both rupture and nonrupture groups. Mean heart weights for men (479 vs 526 g) and women (399 vs 432 g) with and without rupture also were insignificantly different. LV scar before the infarct that ruptured was present in 18 patients (13%); previous necropsy studies of fatal AMI without rupture have indicated that 50% have LV scars. The rupture group had a significantly more frequent (p less than 0.01) lateral wall location of the infarct (12 vs 2%). The number of 3 major (right, left anterior descending and left circumflex) epicardial coronary arteries narrowed at some point greater than 75% in cross-sectional area by atherosclerotic plaque was significantly lower (p less than 0.01) in the rupture group (39 vs 58%). The percent of these 3 arteries totally occluded or nearly so (greater than 95% in cross-sectional area) by plaque also was significantly less (p less than 0.001) in the rupture group (24 of 198 arteries [12%] vs 38 of 144 arteries [26%]). Analysis of each 5-mm long segment of these arteries in each group disclosed that the rupture group had significantly less narrowing than the nonrupture group. Of the 3,287 five-mm segments of artery examined in the rupture group (66 patients), 512 (15%) were narrowed greater than 75% in cross-sectional area by plaque; in contrast, of the 1,848 five-mm segments in the nonrupture group (38 patients), 508 (28%) were narrowed to this degree by plaque (p less than 0.0001). Thus, rupture of the LV free wall primarily is a complication of the first AMI and is associated with considerably less amounts of coronary narrowing than fatal AMI without rupture.

Aged↗
PubMed2005

Use of combination evidence-based medical therapy prior to acute myocardial infarction (from the National Registry of Myocardial Infarction-4).

Utilization rates of aspirin, beta blockers, angiotensin-converting enzyme inhibitors, and statins singly and as part of a multidrug regimen before hospitalization were measured in 109,540 patients with a history of coronary artery disease presenting with acute myocardial infarction to 1,283 hospitals participating in the National Registry of Myocardial Infarction-4. The profile of patients receiving none or only 1 of these therapies was compared with that of patients receiving any 3 or all 4 agents. Most patients (58%) with a history of coronary artery disease presenting with acute myocardial infarction were on none or only 1 of these effective medications at hospital admission. Only 21% of patients were on >or=3 of these therapies. Older age, female gender, and Medicare or no insurance coverage was significantly associated with previous receipt of or=3 of these therapies. In conclusion, data from this large national registry have indicated that most patients with a history of CAD were not receiving the recommended combination of cardiac medications before their AMI.

Adrenergic beta-Antagonists↗