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PubMedDate not supplied

[Anterior infarction of the left ventricle and infarct of the posterior wall of the right ventricle caused by thrombosis of the anterior interventricular artery].

The association: anterior infarction of the left ventricle-posterior infarction of the right ventricle, is a rare entity. The authors report the case of a 64 year-old woman, who died on the fifth day of an extended anterior myocardial infarction, present on electrocardiograms; there were however immediate signs of right heart failure unexplained by a pericardial effusion. At the autopsy, the unusual length and distribution of the anterior interventricular artery which was completely obstructed near its origin by a thrombosis occurring on a severe atheromatous and calcified stenosis, explain this association.

Coronary Disease↗
PubMed1988

Changes in magnesium, zinc, calcium, potassium, cholesterol, and creatine kinase concentrations in patients from pre-infarction syndrome to fatal myocardial infarction.

We measured changes in concentrations of magnesium, zinc, calcium, potassium, cholesterol [total and high-density lipoproteins (HDL)], total creatine kinase (CK), and CK isoenzyme-MB in plasma (PI) and/or erythrocytes (Erc) from apparently healthy subjects and from patients with either pre-infarction syndrome (PIS) or myocardial infarction (MI) with a favorable (MI1) or fatal (MI2) outcome, to assess the relationship of these changes to the increasing severity of ischemic disease. Significant sex-related differences led us to study men and women separately. In MI1 and MI2 patients, concentrations of Mg in PI and Erc were increased as a function of time since the infarct, confirming the cardiac Mg leaves the heart and enters the circulatory compartment. Compared with concentrations in MI2 patients, Zn concentrations in PI were lower in MI2 patients in the days before death. Significant negative correlations between Zn in PI in MI1 men or Zn in Erc in MI2 men and CK or CK isoenzyme MB suggest that circulating Zn is taken up by non-necrotic myocardial tissue as part of the repair process. MI2 patients had gradually decreasing Ca concentrations in PI even more marked than those observed in PIS and MI1 patients. We also noted a marked decrease in total and HDL cholesterol concentrations in both MI2 men and MI2 women shortly before death.

Adult↗
PubMedDate not supplied

Glucose, insulin and platelet fatty acids following myocardial infarction: an association with infarct size.

Fifty-four patients were studied immediately after myocardial infarction to determine the association between infarct size and blood glucose, serum insulin, plasma lipids and platelet phospholipid fatty acids. Infarct size was estimated indirectly from peak plasma lactate dehydrogenase level and in the known diabetics a significant negative correlation was seen between serum insulin and peak LDH levels (Rs = -0.73, p less than 0.05). In the normoglycaemic patients peak LDH level was inversely associated with platelet phospholipid linolenic acid (C18: 3 w3) (Rs = -0.59, p less than 0.01) and with eicosapentaenoic acid (C20: 5 w3) (Rs = -0.51, p less than 0.05). This association may be explained by the role of these fatty acids in platelet aggregation but the potentially protective effect of these fatty acids appears to be lost in diabetic and hyperglycaemic patients.

Blood Glucose↗
PubMed1987

[ECG and coronarographic signs of an anterior wall myocardial infarct accompanied by a right ventricular infarct in the rehabilitation phase].

QRS-complex and ST-segment were analyzed by ECG using 12 routine leads in three right chest wall leads (V3R, V4R, V5R) in patients with chronic anterior wall myocardial infarction. A QRS-complex was found in leads V3R and V4R in proximal occlusion of the LAD in all (n = 22) but four patients, where retrograde filling of the septal branch of the LAD was observed. When the medial LAD was occluded (n = 13), rS-complex was present in the right chest wall leads. Similar ECG findings were revealed in normal coronary arteries (n = 46). QS-complex in leads V3R and V4R refers to right ventricle infarction in the chronic phase of anterior wall myocardial infarction, when the proximal LAD is occluded.

Adolescent↗
PubMed1985

[Reversible asynergy in acute transmural myocardial infarction: evaluations of patients with inferior infarction].

To evaluate the significance of chronological changes in wall motion abnormalities, echocardiography was performed for 46 patients with acute transmural inferior myocardial infarction without previous infarction or complications. Asynergy was analyzed by two-dimensional echocardiography (2-D Echo) on the third day (acute stage) and the 28th day (convalescent stage) after the onset of infarction. Asynergy was quantitatively estimated by dividing the left ventricle into 17 segments. The degree of asynergy was graded on a four-point scale as dyskinesis = 3, akinesis = 2, hypokinesis = 1, and normokinesis = 0. The total wall motion score (TWMS) was calculated on the both days. Improvement of asynergy was observed in 39 cases (84.8%). Among them, both the extent and degree of asynergy were improved in 17 cases (37.0%). In 10 cases (21.7%) the extent of asynergy was reduced. In the remaining 12 cases (26.1%), only the degree of asynergy was decreased. Concerning the relationship between the degree of asynergy on the 3rd day and the subsequent alteration of asynergy on the 28th day, two of four dyskinetic segments still had dyskinesis, and the other two reverted to akinesis. Among 156 akinetic segments, 80 did not change, but 58 reverted to hypokinesis and 18, to normokinesis. Among 82 hypokinetic segments, 48 did not change, but 34 became normal. The relationship between severity of asynergy on the third day indicated by the total wall motion score (TWMS 3rd) and the improvement in the score on the 28th day (TWMS 28th) was investigated in three patient groups: group-A (n = 19) showed TWMS 3rd greater than 9; group-B (n = 22), 9 greater than or equal to TWMS 3rd greater than or equal to 3; group-C (n = 5), TWMS 3rd less than 3. The frequency of "no improvement" was slightly higher in the group-C (62.5%) than in the group-A (52.1%) and in the group-B (56.4%). On comparison, improvement of asynergy was observed in the group-A in 47.9% and in the group-B in 43.6%, but the rate of resolution of asynergy was higher in group-B (53.6%) than in the group-A (40.3%). In the group-C, there was no case of significant coronary artery stenosis greater than 75% in diameter and sigma CPK was smaller than in the other two groups (p less than 0.005).(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1979

Estimation of size of infarcted focus by spatial quantitative vectorcardiography in patients with acute anterior myocardial infarction.

The study included 113 patients with acute myocardial infarction of the left ventricular anterior wall. The patients were repeatedly followed up from the first hours of the affection onward in the course of the individual stages of treatment (stage of intensive monitoring and therapy; intermediate stage; initial rehabilitation with application of active therapy; early mobilization, activation and rehabilitation). A new approach to the estimation of the size of the infarcted focus is described, namely, the method using spatial quantitative vectorcardiography. It was found that the spatial localization of the 40-ms vector, especially its azimuth, is a specific indicator, with the aid of which the localization, extent and depth of the lesion in the left ventricular anterior wall can be assessed with a high probability in most instances. The compensatory adaptive and reparative capacity of the affected myocardium, estimated on the basis of spatial quantitative VCG, is closely correlated with the size of the infarcted focus.

Humans↗
PubMed1984

[Incidence and course of complex ventricular arrhythmias in myocardial infarct as a function of infarct size, heart function and persistent ischemia].

Incidence and course of complex ventricular ectopic activity (VEA) after myocardial infarction was prospectively evaluated in 217 patients in relation to infarct size, location, ventricular function and signs of persistent ischemia. Complex VEA (Lown greater than III) was found acutely in 138 patients (63.6%) and at hospital discharge in 42 (19.3%). Of 79 patients with VEA Lown less than or equal to III in the first 24 hours, 93.7% remained VEA-free at follow-up. Patients with persistent complex VEA differed from those who became VEA-free only in left and right ventricular ejection fraction, whereas all the other infarct related factors had no influence on the course of VEA.

Aged↗
PubMed1983

Reduction in infarct size, arrhythmias and chest pain by early intravenous beta blockade in suspected acute myocardial infarction.

Four hundred seventy-seven patients suspected of having had acute myocardial infarction within less than 12 hours were randomized to receive i.v. atenolol followed by oral treatment for 10 days or to a control group. In patients with ECG changes indicative of infarction at entry, i.v. atenolol significantly reduced enzyme release by one-third and enhanced R-wave preservation. In patients without such ECG changes, treatment significantly prevented the development of infarction in a proportion of patients. There was also a significant reduction in R-on-T ectopics, repetitive ventricular arrhythmias and supraventricular arrhythmias. Treated patients had significantly greater pain relief and required fewer opiate analgesics. Significantly fewer atenolol-treated patients died by 10 days (the treatment period), had nonfatal cardiac arrests, developed heart failure, or suffered reinfarction.

Administration, Oral↗
PubMed1982

[Cross-sectional echocardiographic visualization of the infarcted site in myocardial infarction: correlation with electrocardiographic and coronary angiographic findings].

Three dimensional assessment of the site of myocardial infarct was performed using cross-sectional echocardiography in 68 patients with old myocardial infarction. Patients with a history or electrocardiographic findings suggestive of double or multiple infarctions were excluded from the study. In patients with abnormal Q waves in V1 to V3, a regional wall motion abnormality (asynergy) was observed in the anterior portion of the interventricular septum (IVS) and the anterior free wall of the left ventricle (LV) which was extended from the base to apex. Most of them had a significant stenosis in the left anterior descending artery (LAD) distal to the first diagonal branch. Patients with Q waves in V1 to V5 or V6 showed extensive asynergy in the anterior IVS, anterior and lateral free walls of the LV extended from the base to apex. LAD stenosis proximal to the first diagonal branch seemed to be the corresponding coronary lesion. In patients with Q waves in V3 to V5 or V6, asynergy was limited to the apical half of the anterior wall of the LV. In patients with Q waves in II, III and a VF, asynergy was observed in the basal half of the posterior wall and the posterior portion of the IVS.

Coronary Angiography↗
PubMed1981

[Markers of necrosis and anoxia in the post-infarct heart failure: determination of infarct size (author's transl)].

28 patients with acute myocardial infarct (AMI), 10 of whom presenting left ventricular failure, have been studied. By serial determinations of alpha-hydroxybutyrate dehydrogenase (HBDH) and creatine kinase (CK), the releasing times (RT) and the total releases (TR) of the two enzymes have been calculated, according to the Shell's method modified by Norris. The RT of HBDH have resulted more prolonged in the decompensated patients (48.1 +/- 16.0 vs 37.3 +/- 9.1 h; t = 2.297; p less 0.05). Highly significant correlations have been demonstrated between the total releases of the two enzymes; r = 0.816, p less than 0.01 (with failure); r = 0.766, p less than 0.001 (without failure). For neither enzyme, instead, significant differences have been shown between the TR of the two patient groups. The following conclusions can be drawn. 1) infarct size probably is not the only factor able to induce heart failure during AMI; 2) infarct size can be equally calculated from both HBDH or CK values, though some considerations may make preferable the choice of CK; 3) the more prolonged release of HBDH during heart failure suggests the hypothesis that lactate accumulation is an important factor influencing the appearance of this compliance.

Adult↗
PubMed1995

[A clinical study on limitation of infarct size by ischemic preconditioning in 100 cases of acute myocardial infarction].

The protective effect of ischemic preconditioning has been confirmed in animal models. In this study we analyzed the clinical data of 110 cases of acute myocardial infarction (77 male, 33 female). Sixty-nine cases (group A) had ischemic manifestations prior to myocardial infarction, while forty one (group B) did not have. Our data showed that the clinical features in group B were quite different as compared with those in group A: (1) larger infarct size (ratio between necrotic size and ischemic size: 71.55 +/- 3.70 to 41.65 +/- 3.96, P < 0.0001); (2) higher peak level of serum cardiac enzymes (CPK: 2085.78 +/- 265.57 to 1329.80 +/- 189.44, P < 0.01; CK-MB: 102.73 +/- 12.47 to 47.38 +/- 8.83, P < 0.01); (3) poorer cardiac function [LVEF < 0.45: 12/41 (29.3%) to 6/69 (8.7%), P < 0.05]; (4) higher incidence of left ventricular aneurysm [9/41 (22.0%) to 3/69 (4.3%), P < 0.05] and (5) higher mortality rate in 4 weeks [6/41 (14.6%) to 2/69 (2.9%), P < 0.05]. The difference between the two groups is statistically significant. In addition, the effect of the duration of preconditioning on protection of myocardium, the potential mechanism of preconditioning and its clinical significance were discussed.

Aged↗
PubMed1995

[Two-color flow cytometry analysis of lymphocyte subsets in patients with acute myocardial infarction and post-myocardial infarction syndrome].

Serial changes in lymphocyte subsets were analyzed in 37 patients with acute myocardial infarction (AMI), in 2 patients with postmyocardial infarction syndrome (PMIS), and in healthy subjects (control group) using two-color flow cytometry to investigate cellular immunity after AMI and PMIS. Peripheral blood lymphocyte subsets were measured on admission and at weeks 2, 4, 8, and 16 after the onset of AMI. The white blood cell count was significantly higher on admission and at week 2 in the AMI group compared with the control group. The percentage of CD4-positive helper T cells was significantly higher on admission and at weeks 2 and 4 in the AMI group compared with the control group, and the percentage of CD8-positive suppressor T cells was significantly lower in the AMI group at week 2 than in the control group. The ratio of helper-to-suppressor T cells peaked 2 weeks after the AMI and then decreased gradually. There were no significant changes in the CD4/CD8 ratio, the percentage of cytotoxic T cells, or the percentage of inducer T cells, throughout the observation period. There were no significant differences in the percentage of T cells, B cells, CD4-positive T cells, CD8-positive T cells, and natural killer cells between AMI patients and control subjects. The percentage of activated CD4- and CD8-positive cells was higher in the AMI group at weeks 4 and 8 than in the control group. There was no significant correlation between changes in lymphocyte subsets and infarct size. The percentage of activated CD8-positive cells was consistently higher in the PMIS group compared with the control and AMI groups. The percentage of cytotoxic T cells in one of the PMIS patients was significantly higher than in the AMI group. There were no significant differences in the proportions of other subsets between PMIS and AMI patients. The changes in lymphocyte subsets observed in patients with AMI suggested that immunological competence was enhanced in these patients. Abnormalities in humoral immunity, such as the appearance of anticardiac antibody, have been observed in patients with PMIS. Our results suggest that PMIS is also associated with changes in cellular immunity.

Adult↗
PubMed1995

[M-mode echocardiographic evaluation of contractility and distensibility of infarcted area in patients with inferior myocardial infarction].

The relationship between degree of myocardial damage and distensibility and contractility of the infarcted area was evaluated by M-mode echocardiography. Echocardiography was performed to evaluate the left ventricular inferior wall motion in 33 patients with myocardial infarction (MI) at mean 87.03 days after onset. Exercise 201Tl single photon emission computed tomography (SPECT) was also performed. Eighteen non-MI subjects were analyzed as a control group. Percentage Tl uptake (% TU) of the infarcted area, calculated from SPECT scans, was positively correlated with the mean systolic inferior wall velocity (mSIWV), and with the mean diastolic inferior wall velocity (mDIWV) (r = 0.36, p < 0.05; r = 0.47, p < 0.01, respectively). These data indicate that both velocities were decreased in proportion to the degree of myocardial damage. The patients with MI were divided into two groups based on % TU determined by SPECT. Group I consisted of 17 patients with % TU > or = 60%, and group II 16 patients with % TU < 60%. The patients in group I were diagnosed as having slight myocardial damage, and no relationship between % TU and mSIWV or mDIWV was observed. All patients in group II were diagnosed as having severe myocardial damage, and % TU was closely correlated with mSIWV (r = 0.72, p < 0.01) and with mDIWV (r = 0.70, p < 0.01). All patients in both MI groups displayed a slower mDIWV than the the control subjects (p < 0.05 for group I and p < 0.01 for group II).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Clinical features and long-term outcome of non-Q wave myocardial infarction in the elderly: comparison with Q wave myocardial infarction].

The clinical features and long-term outcome of non-Q wave myocardial infarction (NQMI) in the elderly were assessed in 24 patients with NQMI and compared with those in 48 patients with Q wave myocardial infarction (QMI). NQMI patients had a significantly lower maximal peak of serum creatine phosphokinase activity and lower incidence of pump failure during the acute phase. In-hospital mortality did not differ significantly between the NQMI and QMI patients. Evaluation of acute-phase coronary angiographic features within 6 hours of onset found a significantly higher incidence of infarct-related vessels in the NQMI patients, but the frequency of multivessel disease and the level of collateral flow did not differ between the two groups. Fifteen of the 24 NQMI patients and 34 of the 48 QMI patients underwent emergency coronary revascularization procedures of percutaneous transluminal coronary angioplasty (PTCA) or intracoronary thrombolysis. Successful recanalization was more frequent and the time to recanalization was shorter in the NQMI patients. The requirement for coronary revascularization (PTCA or coronary artery bypass graft) in the chronic phase for residual stenosis did not differ significantly between the two groups. Left ventricular ejection fractions were significantly better in the NQMI patients. The short- and long-term outcomes in elderly patients with NQMI and QMI were good and did not differ between the two groups, probably reflecting the active performance of revascularization in the acute and chronic phases.

Aged↗
PubMed1994

The ESPRIM trial: short-term treatment of acute myocardial infarction with molsidomine. European Study of Prevention of Infarct with Molsidomine (ESPRIM) Group.

Previous small clinical trials have suggested that treatment with nitric oxide donors in suspected myocardial infarction can reduce mortality by 30-35%. To confirm this finding in a large-scale trial, we compared molsidomine and its active metabolite linsidomine (a nitric oxide donor) with placebo in 4017 patients with acute myocardial infarction. In our trial, patients without signs of overt heart failure (Killip III/IV) were randomly assigned in a double-blind design within 24 h of symptom onset to receive linsidomine 1 mg/h intravenously for 48 h, followed by 16 mg molsidomine by mouth daily for 12 days (n = 2007), or an identical placebo (n = 2010). All other treatments could be used at the responsible physician's discretion with the exception of systematic vasodilator treatment. The molsidomine and placebo groups showed similar all-cause 35-day mortality (168 [8.4%] vs 176 [8.8%] deaths, p = 0.66), and adjustment for baseline variables in a Cox model had no effect. Similarly, we found no difference for long-term mortality (mean follow-up 13 months; 294 [14.7%] vs 285 [14.2%] deaths, p = 0.67). The two groups showed similar frequencies of major and minor adverse events; only headache was significantly more common in the molsidomine group. Changes in treatment practices and the lower risk profile of our study subjects than of participants in previous trials may explain the results. It is still not clear whether nitric oxide donors can improve survival in higher-risk myocardial infarction patients.

Administration, Oral↗
PubMed1994

Use of a standardized heparin nomogram to achieve therapeutic anticoagulation after thrombolytic therapy in myocardial infarction. TIMI 4 investigators. Thrombolysis in Myocardial Infarction.

BACKGROUND: The recently completed Thrombolysis in Myocardial Infarction (TIMI) 4 Study compared three thrombolytic treatment regimens for acute myocardial infarction. The treatment arms included front-loaded recombinant tissue plasminogen activator (rtPA), anistreplase (APSAC), or both, in conjunction with an intravenous bolus of 5000 U of heparin, followed by 1000 U/h. To facilitate anticoagulation, a heparin nomogram was developed to maintain the therapeutic activated partial thromboplastin time at 1 1/2 to 2 times the control value. METHODS: A poll revealed that nine centers made use of the recommended heparin nomogram and six did not, adjusting the heparin dosage according to local practice. Anticoagulation parameters, major hemorrhagic events, and the frequency of heparin interruption were compared between centers that used and did not use the nomogram. RESULTS: Subtherapeutic activated partial thromboplastin time values were noted in 4%, 14%, 29%, 46%, 37%, and 34% of patients 8, 12, 24, 48, 72, and 96 hours, respectively, after heparin treatment was begun. Patients with subtherapeutic values at 24 hours were younger (mean +/- SD, 55.2 +/- 10.6 vs 59.6 +/- 10.6 years, P = .02) and weighed more (86.4 +/- 13.5 vs 78.9 +/- 15.7 kg, P = .007) than patients with therapeutic values. Centers that used the nomogram had significantly fewer subtherapeutic values at 48 and 96 hours. In addition, heparin therapy was interrupted less frequently at centers that used the nomogram (38.1% vs 68.7%, P < .001). Major spontaneous hemorrhage, reinfarction, and reocclusion rates were low and were about the same in the two groups. CONCLUSIONS: The use of a heparin nomogram provided improved anticoagulation in patients treated with thrombolytic therapy for myocardial infarction. Weight- and age-adjusted heparin dosing may provide further improvement in anticoagulation with heparin therapy. Our findings support the need for frequent monitoring of the activated partial thromboplastin time and for a standardized approach to adjusting the heparin dosage.

Aged↗
PubMedDate not supplied

[Anterior septal myocardial infarct impairs cardiovascular function more than inferior septal myocardial infarct].

The functional ability, expressed as percentage of expected oxygen uptake, measured on the tread-mill according to the Bruce protocol, was assessed in 30 patients with anteroseptal, and in 30 patients with inferior myocardial infarction (MI), 4 months after the incident. In comparison to those with inferior MI, the patients with anteroseptal localization exhibited significantly lower values of functional ability (68.37% +/- 14% versus 75.63% +/- 11%, p < 0.05), significantly higher activities of creatine kinase (CK: 894.7 +/- 441 versus 603 +/- 330 IU, p < 0.01), significantly lower left-ventricular ejection fraction (53% +/- 6.4% versus 58.7% +/- 6.3%, p < 0.01) and higher negative correlation between CK and functional ability (r -0.85 versus r -0.72). In conclusion, anteroseptal infarction is associated with a greater decrease in functional ability then the inferior one, which is partly due to more extensive necrosis with greater deterioration in left ventricular contratility; the mere site of infarction is probably also a contributing factor.

Exercise Test↗
PubMed1993

[The twenty-year trend in hospital mortality of acute myocardial infarction in Shanghai and the responsible factors. Shanghai Cooperative Group of Myocardial Infarction].

The hospital mortality rates of patients with acute myocardial infarction admitted to 10 main hospitals in Shanghai during the period of 1970-1989 were compared with those of different time periods (year 1970-1974, 1975-1979, 1980-1984 and 1985-1989) and the results disclosed a decreasing trend in mortality in later years. The distribution of major prognostic factors were compared among patients admitted in different time periods and no trend to naturally reduced infarct severity on admission was found. On the contrary, the predicted hospital mortality derived from the prognostic function tends to increase in 1980s. It is, therefore, concluded that the recent decline in hospital mortality of acute myocardial infarction observed is the result of progress and improvement in medical care. The way through which mortality was decreased was discussed.

Aged↗