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PubMed1991

Effect of zinc sulphate on infarct size in experimental myocardial infarction in dogs.

The effect of zinc sulphate on myocardial infarct size following left coronary artery branch occlusion in dogs was studied. Zinc sulphate (10 mg/kg) was administered po, 24 h and 2 h before coronary occlusion in one group of animals. The area at risk was visualised by methylene blue injected intraventricularly. The infarcted area was visualised by triphenyl tetrazolium chloride staining. The infarct size expressed as a percentage of risk zone was 76.54 +/- 3.01 per cent (mean +/- SE) in the control group and 37.96 +/- 2.20 per cent in the zinc sulphate group (P less than 0.001). Zinc sulphate appears to be a potent prophylactic agent for limiting the size of myocardial infarct in the dogs.

Animals↗
PubMed1990

[Effect of thrombolytic agents on infarct size and left ventricle systolic function in myocardial infarction].

The early intravenous administration of thrombolytic agents in the acute phase of myocardial infarction induces reperfusion of the artery responsible for the necrosis, thereby limiting the size of the infarct and preserving the left ventricular systolic function with consequent reduction of short- or long-term mortality. With the exception of urokinase, these effects have been demonstrated with all thrombolytic agents used so far, including streptokinase, plasminogen tissue activator and anistreplase. Owing to its special pharmacokinetic properties, the latest thrombolytic agent, formerly known as APSAC (anisoylated plasminogen streptokinase activator complex), provides a high arterial reperfusion rate with a low percentage of reocclusion. As a result, the mean size of the infarct is reduced by 31 per cent (36% in the case of anterior infarct), and the left ventricular systolic function is highly significantly preserved.

Anistreplase↗
PubMed1990

Effect of isosorbide dinitrate on enzymatically estimated infarction size and on clinical condition of the patients of acute myocardial infarction.

With the aim of reducing myocardial infarction size, isosorbide dinitrate (ISDN) was tried in 27 patients of acute myocardial infarction (AMI). There was 11% reduction of infarction size, in the ISDN treated group, in comparison to that of non treated group, though the result was not statistically significant. But, many of the in-hospital complications were significantly less in the treated group. After a critical analysis of the result it was concluded that a statistically insignificant result, as regard reduction of infarction size in AMI, cannot always exclude the utility of a drug therapy in AMI.

Creatine Kinase↗
PubMed1987

[Differential diagnosis: right heart infarct or anteroseptal infarct?].

We report on the case of a patient with typical clinical symptoms and ST-segment elevation in V1-V4 who was diagnosed as having acute anteroseptal myocardial infarction. Coronary angiography revealed a proximal occlusion of the right coronary artery and a patent dominant left coronary artery. After successful thrombolysis with pro-urokinase a transluminal coronary angioplasty of the right coronary artery was performed. The exact analysis of the first electrocardiogram demonstrated that the decrease of ST-segment elevation in V1-V4 should have suggested the diagnosis of right ventricular infarction. This case report demonstrates the potential hazards in distinguishing right ventricular infarction from anteroseptal infarction by electrocardiogram only.

Adult↗
PubMed1987

Emergency coronary bypass grafting for evolving myocardial infarction. Effects on infarct size and left ventricular function.

Emergency aorta-coronary bypass grafting was performed early in the course of evolving myocardial infarction in 48 patients. The time interval between the onset of symptoms and reperfusion was 169 +/- 80 minutes. Quantitative assessment of postoperative thallium 201 myocardial scans in 19 patients revealed a significant salvage of myocardium after surgical reperfusion: The size of the residual infarction was less than 50% of that in a matched, medically treated, prospective control group (n = 39) (p less than 0.05). Postoperative equilibrium-gated radionuclide blood pool studies (technetium 99m) showed an enhanced recovery of regional and global ejection fraction after operation as compared to after medical treatment (p less than 0.05). Ultrastructural evaluation of biopsy specimens obtained during the operation delineated subendocardial necrosis in the majority of cases (72%), but subepicardial necrosis was found in only 6% of instances. Q-wave abnormalities were observed on the postoperative electrocardiogram in 50% of cases. Operative mortality was 0% in low-risk patients (i.e., hemodynamically stable condition, n = 26) and 18% in high-risk patients (i.e., cardiogenic shock including total electromechanical dysfunction, n = 22). Survival rate at 18 months was 92% +/- 4%, and 95% +/- 4% of the survivors were event free. It is concluded that early surgical reperfusion of evolving myocardial infarction limits infarct size significantly, enhances functional recovery, and may be a lifesaving operation in patients having cardiogenic shock associated with unsuccessful resuscitation.

Actuarial Analysis↗
PubMed1985

Failure of intravenous pindolol to reduce the hemodynamic determinants of myocardial oxygen demand or enzymatically determined infarct size in acute myocardial infarction.

Pindolol, a beta blocker with intrinsic sympathomimetic activity, was investigated in a randomised controlled trial of 100 patients presenting within 12 hours of uncomplicated acute myocardial infarction. Pindolol was given intravenously for 24 hours and orally for 48 hours to achieve serum levels above 10 ng/ml. Heart rate and arterial pressure, both systolic and diastolic, fell to a similar degree in actively treated and control patients. There was no significant difference between systolic blood pressure-heart rate product in actively treated and control patients during the first 72 hours of therapy. There was no increased incidence of cardiac failure, bradycardia, or AV conduction disturbance among pindolol-treated patients. Infarct size estimated from cumulative enzyme release did not differ significantly from controls regardless of whether pindolol was given within four hours or between four and 12 hours of symptom onset. However, fewer patients given pindolol within four hours required morphine. Use of pindolol during the acute phase of myocardial infarction did not appear to modify clinical course, hemodynamic determinants of myocardial oxygen demand, or enzymatically determined infarct size.

Adult↗
PubMed1985

Myocardial response to infarction in the rat. Morphometric measurement of infarct size and myocyte cellular hypertrophy.

For determination of the effects of myocardial infarction on the recovery potential of muscle mass in the surviving tissue, ligation of the left coronary artery was performed in 3-month-old rats, and the infarcted ventricles were analyzed morphometrically a month after surgery. Comparisons were made with 4-month-old control rats that underwent sham operations and with 3-month-old control rats that were not operated upon for evaluation of the magnitude of infarct size and discrimination of the relative contribution of tissue growth that occurred in the surviving myocardium solely as a result of the change in age, from 3 to 4 months (postoperative tissue growth, or POTG), from the additional growth induced by infarction (hypertrophic growth, or HG). Coronary occlusion induced a 276-cu mm loss of ventricular tissue volume that corresponded to 43% of the total left ventricular mass, 648 cu mm. Over a 30-day period the remaining 372 cu mm of viable tissue expanded by 90% with an overall volume gain of 334 cu mm. This tissue augmentation consisted of 20% POTG, 67 cu mm, and 80% HG, 267 cu mm. Total myocyte volume increased 89%, from 302 cu mm to 571 cu mm, and average myocyte cell volume per nucleus increased 92%, from 16,500 cu mu to 31,600 cu mu. The expansion of the myocyte mass was the result of a 21% POTG and a 79% HG. Corresponding values for the myocyte population were 19% and 81%.

Age Factors↗
PubMed1972

The second phase of subendocardial infarction--transmural infarction.

Analysing the clinical course of 30 consecutive patients with acute subendocardial myocardial infarction, the authors draw attention to the frequent development of transmural infarction in patients with septal subendocardial infarction. Heparin treatment of subendocardial infarction can prevent the immediate second phase of the disease.

Diagnosis, Differential↗
PubMed1984

Isolated right ventricular infarction followed by posterior left ventricular infarction after a few days.

This report presents a rare case of isolated right ventricular infarction complicated by bilateral occlusive pulmonary embolism apparently due to right ventricular mural thrombus. Only 2 to 3 weeks later an infarct of the posterior wall of the left ventricle finally occurred. The clinical, pathological and electrocardiographic features of the case are discussed. This case shows that right ventricular infarct can occur without a preceding or simultaneous infarct of the left ventricle.

Aspartate Aminotransferases↗
PubMed1984

[Myocardial infarction in the young subject: a medium-term clinical and coronary angiographic study in 40 patients under 36 years of age. Comparison with coronary angiographic data of myocardial infarction in patients after 50 years of age].

A series of 40 myocardial infarctions, occurring in patients under 36 years of age was studied retrospectively (Group I: mean age 31.3 years). The medium term results of coronary angiography in this group were compared with those of 60 myocardial infarctions after 50 years of age (Group II: mean age 56.6 years). Group I had a clear male predominance (92.5%), a high incidence of smoking (69%), hypercholesterolaemia (69%); myocardial infarction was the first manifestation of their disease in 54% and it was often extensive (42%). A comparative angiographic study between the two groups showed: 1) Less widespread lesions in Group I, as assessed by the number of main arteries stenosed (p less than 0.001), the coronary index (p less than 0.01) and the mean coronary score using Friesinger's method (p less than 0.01). 2) A higher incidence of subnormal coronary angiogrammes in Group I (absence of 50% stenosis) (15%) and of single vessel disease (40%): compared with Group II in which multivessel disease was observed in 86.5% of cases. 3) Collateral circulation was less common in Group I (p less than 0.01). On the other hand, a comparative study of regional and global left ventricular function showed no difference between the two groups. Two subgroups were distinguished in Group I: in one subgroup, multiple lesions similar to those found in Group II, suggestive of premature coronary atherosclerosis (52.5%); the other group (47.5%) presented unilocular lesions i.e. focal mono-arterial lesions compatible with other causes of infarction (thrombosis and/or spasm). These patients were younger (p less than 0.05) and had significantly fewer cardiovascular risk factors (p less than 0.01). Despite the fact that the coronary lesions were limited, the myocardial damage was comparable with the other groups as the collateral circulation was much less developed (p less than 0.02). These appearances were only observed in 3.5% of patients in Group II. The study of the angiographic outcomes of these two types of lesions should show a difference and could contribute to the understanding of their mechanisms.

Adult↗
PubMed1984

[Estimation of the infarct size by two-dimensional echocardiography in cases with acute myocardial infarction].

We evaluated clinically the infarct size in addition to left ventricular end-diastolic and end-systolic volumes (EDV, ESV) and ejection fraction (EF) using two-dimensional echocardiography (2-D) and algorithms based on the modified Simpson's rule. EDV, ESV and EF obtained by 2-D and three algorithms were compared with those obtained by left ventriculography in 23 patients with various heart diseases. Correlation coefficients obtained by our and other two algorithms were 0.88, 0.88 and 0.90, respectively, for EDV and ESV (p less than 0.01), and 0.71, 0.60 and 0.84 for EF (p less than 0.01). Myocardial mass of the region showing asynergy (asynergic size) was calculated by the above-mentioned three methods and compared with peak serum CK values in 14 patients with acute myocardial infarction. The correlation coefficient between both values was 0.76 (p less than 0.01) by our algorithm and it was higher than by other two algorithms (0.37 and 0.70). The time course of changes in asynergic size in acute myocardial infarction was studied by the use of 2-D and our algorithm. Asynergic size was significantly larger on the day of the onset (24.9 +/- 2.9 ml, mean +/- SE) than the third (21.5 +/- 2.7 ml) and seventh day (20.7 +/- 3.0 ml) after the onset (p less than 0.01). These results suggest that one can make a quantitative and serial estimation of infarct size as well as left ventricular volume by 2-D and our modified model, and that our algorithm is suitable for the purpose.

Cardiac Volume↗
PubMed1984

[Heart wall rupture in acute myocardial infarct. An autopsy study in comparison with infarcts without rupture].

Among 237 patients who died of acute myocardial infarction (4% of the 5,390 autopsies from 1975 to 1979) 43 cases (18%) with a rupture of the cardiac wall were found. These 43 cases of rupture were compared with 43 non-rupture cases of the same period. In difference to the non-rupture cases the average weight of the heart was smaller. Myocardial scars, additional basic diseases and a lung oedema were rarer; an extended region of the infarction and an anamnestically known chronic ischemic heart disease were observed significantly more frequently. In what respect these and other analysed factors are responsible for the rupture mechanism, cannot be clearly estimated. Apart from a continuing hypertension as well as a relatively smaller weight of the heart and the absence of myocardial scars the extension of the area of the infarction as well as the possible effect of granulocytic enzymes in the area of the infarction appear significant for the origin of a heart rupture.

Adult↗
PubMed1980

Post-infarction ventricular septal rupture combined with acute right ventricular infarction. A case report.

An elderly White woman suffering from an acute transmural inferior myocardial infarction, with possible true posterior extension, is presented. Her holosystolic cardiac murmur and hypotension are attributed to rupture of the interventricular septum which occurred between the 2nd and 3rd days after infarction. Strong evidence for concomitant right ventricular infarction is put forward and therapy is discussed. As far as the authors can determine, this combination of cardiac lesions has not been documented ante mortem previously. The apparent beneficial use of intravenous hydrallazine, for the first time in right ventricular infarction, is discussed.

Aged↗
PubMed1980

The aspirin myocardial infarction study: final results. The Aspirin Myocardial Infarction Study research group.

The Aspirin Myocardial Infarction Study (AMIS) was a multicenter, randomized, double-blind, placebo-controlled trial of 1.0 g of aspirin daily in men and women who had had a documented myocardial infarction. In the trial 4524 persons, ages 30-69 years, were recruited; 2267 were randomized to aspirin and 2257 to placebo. The major end point, total mortality, was 10.8% in the aspirin group and 9.7% in the placebo group. There was a nonsignificant trend indicating a lower incidence of nonfatal myocardial infarction in the aspirin group (6.3%) compared with the placebo group (8.1%). Symptoms suggestive of gastrointestinal irritation appeared in 23.7% of the aspirin group and in 14.9% of the placebo group. Based on these findings, routine use of aspirin after myocardial infarction is not recommended.

Aspirin↗
PubMed1981

Effect of left ventricular--to--aortic bypass on infarct size and infarct microcirculation in baboons.

A major diagonal branch of the left anterior descending coronary artery (LAD) was acutely occluded in 17 baboons. Complete left ventricular (LV) decompression was achieved with a left heart bypass (LHB) system in six baboons while 11 baboons served as untreated controls. In the treated group, LHB was initiated after 30 minutes of coronary occlusion. For a period of 6 hours after occlusion, aortic pressure, LV pressure, left atrial pressure, and cardiac output were monitored. During the same monitoring period, electrograms were recorded from a high resolution matrix of fixed epicardial electrodes. Regional myocardial blood flow was determined prior to and at intervals following the initiation of LHB with radioactive microspheres. Infarct size was assessed histologically from serial cross sections of the left ventricle. The degree of salvage achieved by LHB was assessed by comparing the epicardial area of infarction 6 hours after occlusion (AI) to the area of epicardial St-segment elevation (STE) 30 minutes after occlusion (maxAST). In the LHB-treated group, 40.0% +/- 8.1% (SEM) of maxAST showed subsequent infarction; in the control group, 79.8% +/- 2.7% of maxAST showed eventual infarction (p less than 0.01). STE overlying the region of ischemia in the LHB-treated group did not undergo the spontaneous decline observed in the control group, which is normally associated with the progression of necrosis. Regional myocardial blood flow did not change significantly in the ischemic region during the period of occlusion following LHB. LHB. The results suggest that LHB is capable of substantial salvage of acutely ischemic myocardium by reducing myocardial work and thus reducing myocardial oxygen requirements.

Animals↗
PubMed1994

[Prevention of post-infarction remodelling with L-carnitine: multicenter study CEDIM (L-Carnitine digital echocardiography myocardial infarction)].

Prevention of post-infarction ventricular remodeling is an important therapeutic aim since left ventricular dilatation is one of the most important prognostic post-infarction determinants. Early reperfusion and chronic treatment with ACE-inhibitors are able to limit remodeling by means of two distinct mechanisms. Early reperfusion limits the extent of the infarcted area by salvaging a part of the myocardial area at risk of necrosis. ACE-inhibition, on the other hand, by reducing afterload, facilitates cardiac ejection and therefore tends to reduce left ventricular volume. Remodeling could be limited also by drugs which, like L-carnitine, act, as has been demonstrated by experimental studies, on the use of energy substrates both in the area at risk of necrosis and in the area subjected to a greater wall stress because of remodeling and which will progressively dilate over time. The CEDIM study is a double-blind, randomized, placebo-controlled, multicentre trial which has involved 36 Heart Divisions. The CEDIM study aims at evaluating the effects of L-carnitine on left ventricular function, as assessed by echocardiography, in patients with acute anterior myocardial infarction.

Carnitine↗
PubMed1993

Effect of ramipril on mortality and morbidity of survivors of acute myocardial infarction with clinical evidence of heart failure. The Acute Infarction Ramipril Efficacy (AIRE) Study Investigators.

Survival after acute myocardial infarction has been enhanced by treatment with thrombolytic agents, aspirin, and beta-adrenoceptor blockade. However there remains a substantial subgroup of patients who manifest clinical evidence of heart failure despite the first two of these treatments, and for whom beta-adrenoceptor antagonists are relatively or absolutely contraindicated. These patients have a greatly increased risk of fatal and non-fatal ischaemic, arrhythmic, and haemodynamic events. In this selected high-risk subset of patients we investigated the effect of therapy with the angiotensin converting enzyme (ACE) inhibitor rampiril, postulating that it would lengthen survival. 2006 patients who had shown clinical evidence of heart failure at any time after an acute myocardial infarction (AMI) were recruited from 144 centres in 14 countries. Patients were randomly allocated to double-blind treatment with either placebo (992 patients) or ramipril (1014 patients) on day 3 to day 10 after AMI (day 1). Patients with severe heart failure resistant to conventional therapy, in whom the attending physician considered the use of an ACE inhibitor to be mandatory, were excluded. Follow-up was continued for a minimum of 6 months and an average of 15 months. On intention-to-treat analysis mortality from all causes was significantly lower for patients randomised to receive ramipril (170 deaths; 17%) than for those randomised to receive placebo (222 deaths; 23%). The observed risk reduction was 27% (95 % Cl 11% to 40%; p = 0.002). Analysis of prespecified secondary outcomes revealed a risk reduction of 19% for the first validated outcome (i.e., first event in an individual patient)--namely, death, severe/resistent heart failure, myocardial infarction, or stroke (95% Cl 5% to 31%; p = 0.008). Oral administration of rampiril to patients with clinical evidence of either transient or ongoing heart failure, initiated between the second and ninth day after myocardial infarction, resulted in a substantial reduction in premature death from all causes. This benefit was apparent as early as 30 days and was consistent across a range of subgroups.

Adult↗
PubMed1993

Cumulative enzyme release as a measure of infarct size in patients with acute myocardial infarction receiving thrombolytic therapy.

Infarct size can be assessed in patients with myocardial infarction by calculating cumulative enzyme release. The two compartment model is used in patients who received thrombolytic therapy as well as in patients who were not treated with thrombolytic agents. The most practical approach is to calculate cumulative release of lactate dehydrogenase (LDH). Blood samples have to be obtained twice daily during the first two days, and once daily during day three to five. Cumulative LDH release can then be calculated with help of a simple computer program, presently available for use on a PC. Cumulative enzyme release was calculated from the patients who were included in the study with intracoronary streptokinase conducted by the Intervuniversity Cardiology Institute of the Netherlands, in the trial conducted by Anderson, in the ISAM study, and in the trial with rt-PA versus placebo that was coordinated by the European rt-PA study group. In all studies it was demonstrated that thrombolytic therapy led to a limitation of infarct size (less cumulative enzyme release) when compared to controls. In future trials calculation of cumulative enzyme release will have to be incorporated in the design of those trials in which the effectiveness of proposed new therapeutic regimens (like acute PTCA) is tested in patients with acute myocardial infarction and will be compared to the nowadays "standard" therapy with thrombolytic agents.

Acute Disease↗