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At least 811 records · Page 45Linked to original sources
PubMed1978

Effects of pharmacological intervention on infarct size following induced myocardial infarction in rats.

Several therapeutic agents that alter infarct size were administered to rats with myocardial infarcts induced by electrocauterization. The myocardial tissue damage and infarct size correlated well with the creatine phosphokinase myocardial band activity, and these markers were utilized to assess the action of the therapeutic agents on myocardial tissue damage. Hyaluronidase, insulin, potassium chloride, and isoproterenol increased myocardial tissue damage whereas heparin and prednisolone administration resulted in decreased myocardial tissue damage after induced myocardial infarction in rats.

Animals↗
PubMed1997

Myocardial function in infarcted and remote regions early after infarction in man: assessment by magnetic resonance tagging and strain analysis.

Early after infarction in the perfusion bed of the left anterior descending coronary artery, cine MRI with spatial modulation of magnetization (SPAMM) tagging (7-mm grid) was used for short- and long-axis cardiac imaging. Two-dimensional strain analysis of triangular finite elements was performed between end-diastole and end-systole. Patients (n = 10) were compared with age-matched healthy subjects (n = 8). The anteroseptal region at midventricular level was considered representative for "infarcted" and the posterolateral region at basal level was considered "remote". The left ventricular end-diastolic volume index was larger in the patients (69 +/- 15 ml/m2 versus 56 +/- 4 ml/m2, P < 0.05). Short-axis images showed in the infarcted region a decrease of first principal strain (greatest systolic lengthening: 1.10 +/- .06 versus 1.27 +/- 0.04, P < 0.0001), and in the remote region an increase (1.48 +/- 0.11 versus 1.36 +/- 0.07, P < 0.025). The lateral and inferior ventricular regions at mid- and basal levels were found to function normally. Long-axis images yielded similar results. Early after infarction, regions with dysfunction, normal function, and hyperfunction can be delineated with MR tagging. The compensatory increased contraction in the remote region is possibly triggered by the Frank-Starling mechanism.

Case-Control Studies↗
PubMed1983

Experimental right-ventricular infarction in rats by abdominodiaphragmal access to the heart. A new technique in the study of infarcted myocardium.

An abdominodiaphragmal way of producing right-ventricular myocardial infarction is introduced, allowing of ligation of the right-coronary artery and vein without further manipulation of the heart. Of the rats operated upon, 22% died perioperatively. Of the surviving part, 89% had myocardial infarction macroscopically. This method was used to study enzyme decreases in infarcted myocardium. Our biochemical results correlate very well with histological and histobiochemical findings reported by other investigators. Therefore, we conclude that right-coronary artery ligation in rats by transabdominal, transdiaphragmal access to the heart can be a useful way to study biochemical aspects of infarcted myocardium.

Animals↗
PubMed2000

Life-saving strategy for left ventricular free wall rupture after acute myocardial infarction. Infarction-covering repair on the ruptured site under the beating heart.

OBJECTIVE: Left ventricular free wall rupture after acute myocardial infarction is a serious complication with high mortality. For life-saving, it is important how to maintain poor hemodynamics till operation. We have consistently made it our strategy to attach percutaneous cardiopulmonary support system and intra-aortic balloon pumping immediately after the diagnosis regardless of the type of left ventricular free wall rupture and of the hemodynamic conditions, and perform an infarction-covering repair under the beating heart. We have studied the short-term and middle-term results after the operations, and have evaluated the efficacy and problems of this procedure. METHODS: Since September 1994, we have performed this method in six of eight patients with left ventricular free wall rupture. RESULTS: As results, five of the six patients (83%) were saved including two cases of blow-out type. Our strategy for left ventricular free wall rupture showed several advantages for preoperative and intraoperative maintenance of the hemodynamic conditions, and for preservation of some reversible myocardium by the simple technique of infarction-covering repair under the beating heart. These resulted in shortening the operation time, decreasing the incidence of low cardiac output syndrome, and obtaining a satisfactory rate of life-saving. CONCLUSION: We believe that this infarction-covering repair based on our strategy is effective for life-saving during the acute period.

Aged↗
PubMed2002

A model of closed chest regional myocardial infarction in the rabbit: a clinically relevant in vivo assay system of post-infarction remodelling.

Coronary artery ligation is the standard technique to induce regional myocardial infarction in small animal models. However, opening the chest and incising the pericardium independently influence post-MI remodelling. Our purpose was to develop and characterize a novel closed chest model of regional myocardial infarction (MI) in the rabbit of increased clinical relevance. Coronary angiography was performed percutaneously in New Zealand White Rabbits (NZW) using pre-formed catheters. A 0.36 mm thrombogenic coil was positioned in the circumflex artery to induce closed chest MI. Of rabbits undergoing coil deployment 40 % survived until day 100. Rabbits were classified as small MI (n = 5), moderate MI (n = 6) and large MI (n = 6) < 15 %, 15 - 30 %, > 30 % of LV myocardial volume respectively) or sham controls (n=11). Transthoracic echocardiographic images were obtained 0, 3, 5, 7, 14, 28, 60, 100 days post procedure. At day 100, LVEDP was measured before and after plasma substitute infusion. Hearts were subsequently excised and chamber stiffness (Kc) was derived from the passive pressure-volume relationship. Cardiac weight, dimensions and MI as a percentage of LV volume (MI%) were also recorded. Differences in percentage fractional shortening (%FS) were apparent from day 14. %FS was reduced in rabbits with large and moderate MI compared to controls (day 100, p < 0.005 and p < 0.05, respectively). LVEDP was increased in large and moderate MI compared to small MI and controls (26 mmHg +/- 6 and 21 mmHg +/- 5 vs. 9 mmHg +/- 1 and 7 mmHg +/- 3 p < 0.005); these differences were maintained during plasma substitute infusion. Kc in large MI was significantly less than moderate MI, small MI or control (all p < 0.05). Direct morphometric measurements distinguished between all groups.This study provides the first description of post-infarction remodelling after coronary artery occlusion where the pericardium remains intact in a small animal model. We believe it may provide a more physiologically and clinically relevant in vivo assay system of left ventricular dysfunction after myocardial infarction.

Animals↗
PubMed1981

Right ventricular infarction: relationships between ST segment elevation in V4R and hemodynamic, scintigraphic, and echocardiographic findings in patients with acute inferior myocardial infarction.

The relationship between ST segment elevation on the right precordial lead V4R and the hemodynamic, echocardiographic, and myocardial scintigrapic signs suggestive of right ventricular (RV) infarction was studied in 42 patients with acute inferior myocardial infarction. Twenty-two patients had ST segment elevation in V4R. Among these patients, a significant correlation was demonstrated between V4R ST segment elevation and the hemodynamic (p less than 0.001), scintigraphic (p less than 0.001), and echographic (p less than 0.02) criteria for acute RV infarction. These results support the validity of this new electrocardiographic sign as a practical means in aiding the clinical detection of RV involvement with acute transmural inferior myocardial infarction.

Acute Disease↗
PubMed1981

Intracoronary streptokinase thrombolytic recanalization and subsequent surgical bypass of remaining atherosclerotic stenosis in acute myocardial infarction: complementary combined approach effecting reduced infarct size, preventing reinfarction, and improving left ventricular function.

In 48 patients with acute myocardial infarction (AMI) the acutely thrombus-occluded coronary artery was successfully recanalized nonsurgically via catheter with intracoronary streptokinase (SK) infusion after a mean occlusion time of 3.1 +/- 1.6 hours. In all cases residual high-grade fixed atherosclerotic stenosis remained after percutaneous transluminal coronary recanalization (PTCR). Subsequent aortocoronary bypass surgery (ACBS) circumventing the stenotic coronary artery was performed during the acute stage of myocardial infarction (within 10 days of AMI onset) in 34 patients and electively (longer than 10 days after AMI onset) in 14 patients. No patient died from early PTCR or from ACBS intervention. There were two late post-ACBS arrhythmogenic deaths, two patients suffered nonfatal reinfarction post ACBS several months after hospital discharge, only two had occasional post-ACBS angina pectoris, and one patient had post-ACBS mild heart failure. The remaining 41 post-ACBS patients were completely asymptomatic throughout long-term follow-up evaluation. In the left ventricular (LV) segment supplied by the initially occluded coronary artery, which was recanalized early by means of SK therapy and subsequently grafted, wall motion improved significantly from the acute to the postoperative stage in patients who underwent early surgery (from 13.6% +/- 1.9% to 40.3% +/- 2.7%, p less than 0.001) and in the electively operated group (from 18.0% +/- 7.1% to 48.2% +/- 6.3%, p less than 0.001). Ischemic wall motion was improved irrespective of whether or not the bypass graft circumventing the residual stenosis of the infarct vessel remained patent. Wall motion of nonischemic segments remained essentially unchanged. In the patients who underwent surgery in the early stage, the closure rate of the bypass graft to the infarct-related vessel was 17%, and in the electively operated group no graft was found to be occluded. In conclusion, coronary artery recanalization, achieved by means of early SK-PTCR therapy with subsequent ACBS, can be performed safely in patients with AMI, and the result will be marked improvement in LV segmental wall motion and global function, diminished reinfarction rate, and reduced incidence of angina pectoris, all benefits that are consistently maintained during long-term evaluation.

Angioplasty, Balloon↗
PubMed1988

Effect of reperfusion on electrocardiographic and enzymatic infarct size: results of a randomized multicenter study of intravenous anisoylated plasminogen streptokinase activator complex (APSAC) versus intracoronary streptokinase in acute myocardial infarction.

The effect of early coronary artery reperfusion on ECG and enzymatic parameters was examined in 240 patients with acute myocardial infarction. These patients had participated in a randomized trial comparing intravenous anisoylated plasminogen streptokinase activator complex (APSAC) (n = 123) and intracoronary streptokinase (n = 117) therapy. Reperfusion occurred in 59 of 115 (51%) patients receiving APSAC and 67 of 111 (60%) patients receiving streptokinase (p = NS). There was greater early resolution of ST segment elevation in the reperfused than in the nonreperfused patients (p less than or equal to 0.003) and more rapid Q wave evolution (p less than or equal to 0.03). Sigma Q was lower in reperfused than in nonreperfused patients at 8 hours (1.41 +/- 1.18 versus 2.11 +/- 2.10 mV; p less than or equal to 0.05) and at 24 hours (1.43 +/- 1.25 mV versus 2.08 +/- 1.88 mV; p less than or equal to 0.02). Time to peak level was shorter in the reperfused patients for creatine kinase (CK) (10.7 +/- 5.5 hours versus 14.9 +/- 5.9 hours; p less than 0.0001) and lactic acid dehydrogenase (LDH) (29.6 +/- 13.6 hours versus 34.4 +/- 10.5 hours; less than or equal to 0.03) enzymes. Peak LDH-1 was lower in the reperfused group (274 +/- 149 U/L versus 341 +/- 173 U/L; p less than or equal to 0.04). Reperfusion at a mean of 3.9 hours after the onset of infarction was associated with more rapid resolution of ST segment elevation, faster Q wave evolution, smaller ECG infarct size, earlier cardiac enzyme release, and smaller enzymatic infarct size than later or no reperfusion.

Anistreplase↗
PubMed1989

Right ventricular infarction: diagnostic value of ST elevation in lead III exceeding that of lead II during inferior/posterior infarction and comparison with right-chest leads V3R to V7R.

The diagnostic accuracy of ST elevation in lead III exceeding that of lead II (ratio III/II greater than 1) in the diagnosis of right ventricular infarction was investigated in 24 autopsied patients with inferior/posterior myocardial infarction on ECG. The results were compared with the diagnostic accuracy of ST elevation greater than or equal to 1 mm in right-chest leads V3R to V7R recorded in the same patients. All had left ventricular infarction documented at autopsy, and 17 (71%) had concomitant right ventricular involvement. The highest specificity (100%) and positive predictive value (100%) were calculated for the right-chest leads, whereas values for ratio III/II greater than 1 were 88% and 91%, respectively. The differences were not statistically significant. It is concluded that differences in ST elevation in leads III and II can be the basis for a diagnosis of right ventricular involvement in ECG-diagnosed inferior/posterior infarction. The diagnosis, however, may be achieved more easily with right-chest leads.

Adult↗
PubMed1990

Assay of serum cardiac myosin heavy chain fragments in patients with acute myocardial infarction: determination of infarct size and long-term follow-up.

To evaluate the correlation between myosin heavy chain release and the necrosis mass, serum levels of myosin heavy chain fragments were determined serially in 55 patients with acute myocardial infarction. Eight of these patients were successfully treated with thrombolytic agents: the others were not treated. The same myosin titration was applied to the sera of 25 dogs with an experimental myocardial infarction. Six of the dogs were successfully treated with thrombolytic agents. The time courses of the myosin concentrations are typical and monophasic for all patients with a noncomplex myocardial infarction. The values for the kinetic parameters of myosin release are comparable to those previously reported. We have now determined that cumulative myosin release significantly correlates with cumulative creatine kinase (CK), CK-MB, and lactate dehydrogenase release, as well as with thallium-201 distribution, as determined for different patient groups. Thrombolytic treatment does not seem to qualitatively upset myosin kinetics. The results obtained in dogs with or without thrombolysis conclusively indicate that myosin release is a quantitative index of the necrosis mass. From a practical point of view, a few serial determinations of serum levels of myosin heavy chains are enough to estimate the necrosed mass in patients with acute myocardial infarction. More generally, serum myosin titration could be useful in detecting any cardiac disturbance involving myocardial injury resulting in membrane leakage of cardiac cells.

Adult↗
PubMed1995

Effect of 100% oxygen administration on infarct size and left ventricular function in a canine model of myocardial infarction and reperfusion.

High oxygen concentrations reduced infarct size in prereperfusion era studies; however, with reperfusion therapy, high oxygen tension carries the theoretical risk of exacerbating reperfusion injury by increasing toxic oxygen-derived free radicals. In this study, two groups of dogs underwent 90 minutes of coronary occlusion and 72 hours of reperfusion. The oxygen group (n = 16) received 100% inspired oxygen from 20 minutes before reperfusion through 3 hours of reperfusion, whereas the room-air group (n = 19) was ventilated with room air. Infarct size (as a percentage of risk area) was reduced by 38% in the oxygen group (26.7% +/- 4.7% vs 43.3% +/- 4.3%; p = 0.017). This benefit was independent of underlying variability in collateral blood flow in individual dogs (p = 0.016 by analysis of covariance [ANCOVA]). Left ventricular ejection fraction was significantly improved in the oxygen group (43% +/- 3% vs 33% +/- 2%; p = 0.008), as was regional function in the infarct zone (p < 0.05). These data suggest that high concentrations of inspired oxygen may also benefit patients with acute myocardial infarction who undergo reperfusion therapy.

Animals↗
PubMed1981

Ventricular fibrillation complicating temporary ventricular pacing in acute myocardial infarction: significance of right ventricular infarction.

Five patients with acute myocardial infarction had ventricular fibrillation as a complication of indicated temporary pacing. All five patients had evidence of right ventricular infarction (three patients with postmortem confirmation). The presence of right ventricular infarction seems to be a contributing mechanism involved in the induction of ventricular fibrillation during temporary pacing for bradyarrhythmia complicating acute myocardial infarction.

Adult↗
PubMed1984

Comparison of left ventricular function and infarct size in patients with and without persistently positive technetium-99m pyrophosphate myocardial scintigrams after myocardial infarction: analysis of 357 patients.

One hundred nine patients with persistently positive technetium-99m pyrophosphate (Tc-99m-PPi) myocardial scintigrams 6 months after acute myocardial infarction (MI) (Group A) and 185 patients without such persistently positive scintigrams (Group B) were compared with regard to enzymatically determined infarct size, early and late measurements of left ventricular (LV) function determined by radionuclide ventriculography, and preceding clinical course during the 6 months after MI. The CK-MB-determined infarct size index in Group A (17.4 +/- 10.6 g-Eq/m2) did not differ significantly from that in Group B (16.0 +/- 14.6 g-Eq/m2). Similarly, myocardial infarct areas in the 2 groups, determined by planimetry of acute Tc-99m-PPi scintigrams in those patients with well-localized 3+ or 4+ anterior pyrophosphate uptake, were not significantly different (35.7 +/- 13.4 vs 34.4 +/- 13.1 cm2, respectively). However, patients in Group A had significantly lower LV ejection fractions than those in Group B, both within 18 hours of the onset of MI (0.42 +/- 0.14 vs 0.49 +/- 0.14, p less than 0.01) and at 3 months after MI, both at rest (0.42 +/- 0.14 vs 0.51 +/- 0.14, p less than 0.01) and at maximal symptom-limited supine bicycle exercise (0.44 +/- 0.17 vs 0.51 +/- 0.17, p less than 0.01). Peak exercise levels achieved in the 2 groups were not significantly different. Furthermore, patients in Group A demonstrated a greater incidence of congestive heart failure during the initial hospital admission (41 vs 24%; p less than 0.01) and a greater requirement for digoxin (p less than 0.05) and furosemide (p less than 0.01) after discharge.(ABSTRACT TRUNCATED AT 250 WORDS)

Ambulatory Care↗
PubMed1988

Relation of left ventricular dilation during acute myocardial infarction to systolic performance, diastolic dysfunction, infarct size and location.

The quantification of left ventricular (LV) volumes and assessment of their relation to systolic and diastolic dysfunction, infarct size and anatomic location were performed in 54 patients with a first acute myocardial infarction (AMI). Blood pool radionuclide angiography was used to assess LV end-diastolic, end-systolic, and stroke volume indexes, ejection fraction and peak diastolic filling rate. Infarct size was estimated from plasma MB creatine kinase activity. Substantial LV dilation occurred within the initial 24 hours of AMI. The peak diastolic filling rate was low, even in those patients with a normal ejection fraction. In comparison with inferior AMI (n = 25), patients with anterior AMI (n = 29) had a larger end-diastolic volume index (105 +/- 8 vs 81 +/- 4 ml/m2, p less than 0.01) and end-systolic volume index (64 +/- 7 vs 37 +/- 4 ml/m2, p less than 0.001), but similar stroke volume index (41 +/- 3 vs 43 +/- 2 ml/m2, difference not significant). No significant relation was noted between infarct size estimated by MB creatine kinase and any volumetric index. On repeat study (day 10 after AMI), end-diastolic and end-systolic volume indexes increased further (p less than 0.05 vs day 1) but ejection fraction and peak diastolic filling rate were unchanged. It was concluded that: (1) LV dilation occurs within hours of AMI in both inferior and anterior AMI, but is more marked in the latter; (2) significant LV diastolic dysfunction is the rule, even in patients with preserved LV systolic function; and (3) LV dilation is an early compensatory mechanism that maintains normal stroke volume, even in patients with severely reduced LV function.

Cardiac Volume↗
PubMed1989

Angiographic characteristics of the infarct-related coronary artery in patients with angina pectoris after myocardial infarction.

To elucidate the pathophysiology of angina pectoris after myocardial infarction, we analyzed the coronary stenoses in 45 subjects (28 men, 17 women, aged 33 to 67 years) with recent (less than or equal to 60 days) infarction, significant narrowing of only the infarct-related artery, and residual anterograde flow in this artery. Postinfarction angina was absent in 19 (group I) and present in 26 (group II). The groups were similar in age, left ventricular function, incidence with which each coronary artery was involved, as well as stenosis diameter (1.0 +/- 0.3 vs 0.9 +/- 0.4 mm [mean +/- standard deviation], respectively, difference not significant), stenosis area (0.9 +/- 0.4 vs 0.8 +/- 0.8 mm2, respectively, difference not significant), percent diameter narrowing (65 +/- 5 vs 66 +/- 9, respectively, difference not significant), and stenosis eccentricity. However, those with postinfarction angina had longer stenoses (group I, 4.3 +/- 1.4 mm; group II, 10.3 +/- 4.0 mm; p less than 0.001). Thus, patients with postinfarction angina and residual anterograde flow in the infarct artery may have angina due to a marked reduction in anterograde flow, caused by a long stenosis. There is no apparent relation between stenosis eccentricity and postinfarction angina.

Adult↗
PubMed1989

Qualitative and quantitative comparison of amounts of narrowing by atherosclerotic plaques in the major epicardial coronary arteries at necropsy in sudden coronary death, transmural acute myocardial infarction, transmural healed myocardial infarction and unstable angina pectoris.

The amounts of narrowing of the 4 major (left main, left anterior descending, left circumflex and right) epicardial coronary arteries by atherosclerotic plaques were compared in 4 subsets of coronary patients. Of the 129 patients studied at necropsy, an average of 2.7 of the 4 arteries was narrowed greater than 75% in cross-sectional area at some point (0.7/4 in controls), and the group with unstable angina pectoris (3.2/4) had more narrowing than did the groups with sudden coronary death (2.8/4), acute myocardial infarction (2.7/4) and healed myocardial infarction (2.3/4). Each of the 4 major epicardial coronary arteries was divided into 5-mm long segments and a histologic section was prepared and stained by the Movat method of each of the 6,461 segments in the 129 patients and in the 1,849 segments in the 40 control subjects. In the 129 patients, 35% of the 5-mm segments were narrowed 75 to 100% in cross-sectional area (3% in controls) and the group with unstable angina had the highest percent (48%) of segments severely narrowed compared to the groups with sudden coronary death (36%), acute myocardial infarction (34%) and healed myocardial infarction (31%). Thus, of the 4 subsets of patients with fatal coronary artery disease studied at necropsy, those with unstable angina pectoris had the most severe and extensive coronary atherosclerosis.

Angina Pectoris↗
PubMed1991

Prognostic importance of collateral flow and residual coronary stenosis of the myocardial infarct artery after anterior wall Q-wave acute myocardial infarction.

Residual high-grade coronary stenosis and collateral flow are frequent findings in the chronic phase after a Q-wave acute myocardial infarction (AMI). The prognostic importance of a residual stenosis of the infarct artery and of collateral flow to the infarct area was analyzed in a group of 102 young patients (mean age 35 years, range 22 to 39) who had survived an anterior wall Q-wave AMI. Patients whose only significant lesion (greater than 50% luminal diameter reduction) was in the proximal portion of the left anterior descending artery were enrolled in the study. A 50 to 74% diameter stenosis was present in 33 of 102 patients (32%), 43 (42%) had a 75 to 99% stenosis and 26% had a total occlusion of the infarct vessel. Collateral vessels, which were evaluated by a scoring system, were present in 52 of 102 patients (51%). Four percent had only faint (score 1), 17 of 102 patients (17%) had moderate and 32 patients (31%) had good collateral flow (score greater than 4). The 8-year cumulative mortality was 15.2%--an eightfold increase compared with the age-matched general population. No patient with less than 75% stenosis died during follow-up, whereas the cumulative 8-year mortality was 23 and 17% in patients with a 75 to 99% stenosis or total occlusion, respectively (p less than 0.01). Patients with at least moderate collateral flow had a mortality rate of 21%, versus 8% for patients without or with faint collateral flow (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Early and late changes in left ventricular filling after acute myocardial infarction and the effect of infarct size.

To characterize the early (1 week) and late (6 weeks) changes in left ventricular (LV) filling pattern associated with acute myocardial infarction (AMI) 45 patients (mean age 65 +/- 2 years) were studied by Doppler echocardiography. Based on clinical criteria, patients were divided into those with large (group L; n = 12) and those with small (group S; n = 33) infarcts and then compared with 16 age-matched control subjects. The following parameters were calculated from the mitral velocity waveform: (1) peak early and peak atrial velocities and their integrals; (2) peak early to atrial velocity ratio and velocity integral ratio; and (3) the pressure half-time of the early wave. One week after AMI, group L showed a decreased atrial and increased early velocity, velocity ratio and integral ratio, whereas the pressure half-time of the early wave was shorter than that in group S and in control subjects. At 6 weeks group L showed a reduction in early velocity, early to atrial velocity ratio and integral ratio, whereas pressure half-time increased. When groups S and L were combined there was a good inverse correlation between pressure half-time and infarct size as measured by peak enzyme release (r = -0.64, p < 0.001). These data suggest that, depending on infarct size, patients exhibit a "restrictive" filling pattern early after the acute event. This is manifested by the greater proportion of filling occurring in early diastole, reflecting an overall increase in chamber stiffness. At 6 weeks, this pattern is less pronounced presumably due to the remodeling process.

Aged↗