Prediction of right ventricular infarction from standard surface ECG in patients with inferior myocardial infarction.

BACKGROUND: Patients with inferior myocardial infarction (MI) have a 45% chance of having concurrent right ventricular infarction (RVI); of these, 5-10% suffer hemodynamic collapse. Immediate correct diagnosis and appropriate management of such patients is vital. ST-segment elevation in the right precordial V4 lead (V4R) has a high diagnostic value in identifying RVI, but this determination requires additional time and cost. An attempt was made to use a collection of patients' standard surface electrocardiograms (ECG) to find any available data to detect RVI and to lead to a new way to diagnose RVI. METHODS: Fifty patients (males/females, 44/6; mean age, 64.3 +/- 6.9 years) with acute inferior myocardial infarction were enrolled in a first group to develop new diagnostic criteria for RVI. As a first step, the ST-segment change in every standard surface ECG lead was analyzed and compared with corresponding changes in V4R. RVI was diagnosed by typical clinical symptoms (chest pain for more than 30 minutes, ST elevation > 0.1 mV and enzyme changes) accompanying ST elevation of more than 0.1 mV in V4R (by Lopez-Sendon criteria) and echocardiographic findings. RVI was diagnosed in 24 (48%) patients using ECG. The new criteria were then tested in a secondary group of 48 patients (males/females, 43/5; mean age, 65.5 +/- 7.9 years) with inferior MI. RESULTS: Analysis of these patients found that ST depression in lead I and aVL was a specific characteristic of RVI (I + aVL > 0.2 mV). This criterion was applied to another group of patients with acute inferior MI to check the predictive value (sensitivity, 94.7%; specificity, 89.7%; positive predictive value, 85.7%; negative predictive value, 96.3%). CONCLUSIONS: In patients with evolving inferior MI, standard surface ECG analyzed for this criterion could aid clinical recognition of concomitant RVI.

Effect of losartan and captopril on expression of cardiac angiotensin II AT1 receptor mRNA in rats following myocardial infarction.

AIM: To study the effects of losartan (Los) and captopril (Cap) treatment on expression of cardiac angiotensin II (Ang) AT1 receptor mRNA in rats following myocardial infarction (MI). METHODS: Twenty-four rats with MI after coronary ligation for 7 d were randomly divided into 4 groups: A) Cap in drinking water, ad lib (2 g.L-1), B) i.g. Los 10 mg.kg-1.d-1, C) i.g. Los 30 mg.kg-1.d-1, and D) placebo for 6 wk. Sham-ligation rats (group E) served as controls. The levels of cardiac Ang AT1 receptor mRNA expression in each group (n = 6) were examined by Dot blot using digoxigenin-labeled cDNA probes. RESULTS: Comparing with reflected peak areas of hybridization positive signals in group D (2640 +/- 201 micron 2), the expression of the cardiac Ang AT1 receptor mRNA was much lower in the 3 treated groups (group A 1360 +/- 134 micron 2, group B 1430 +/- 244 micron 2, group C 1310 +/- 95 micron 2) (P < 0.01). But no difference was found between the 3 treated groups and sham-ligation group (1230 +/- 233 micron 2) (P > 0.05). CONCLUSION: Los and Cap attenuated the increase of cardiac Ang AT1 receptor mRNA expression in rats following MI.

[Factors predicting mortality in idiopathic dilated cardiomyopathy].

A study of factors predicting mortality was performed in 69 patients with idiopathic dilated cardiomyopathy by analyzing 14 parameters according to clinical, electrocardiographic and echocardiographic findings. On admission 64% of the patients were in NYHA functional class 3 or 4. During a mean follow-up period of 18 months 43 patients died; 31 of refractory heart failure and 12 suddenly. 1 year survival was 58%. Multivariate analysis (Cox model) revealed that the independent predictors for mortality due to refractory heart failure were left ventricular enddiastolic diameter, NYHA functional class and systolic blood pressure; the presence of tricuspid regurgitation predicted mortality due to sudden death.

Tumors of the heart. An analysis of 79 cases.

There were 79 cases of cardiac tumors seen from 1957 to July 1988. 49 (62.0%) of them were benign and 30 (38.0%) malignant. All the 49 benign tumors except 2 were surgically excised and found to be myxoma. Of them, 18 patients were male and 31 female. 85.7% of the tumors were located in the left atrium, 12.2% in the right atrium and 2.0% in the left ventricle. Palpitation, dyspnea, chest oppression, fever, episodes of syncope and hemiplegia, cough, diastolic and systolic murmurs at the apical or tricuspid area were the common symptoms and signs. Atrial fibrillation was found only in 2 cases. Echocardiographic findings were diagnostic while ECG and X-ray findings were nonspecific. Four patients died after operation. Of the 30 cases of malignant tumors, 15 were secondary tumors metastasized mainly from the lung or mediastinal malignancies. Of 11 primary tumor cases (7 males and 4 females), 3 were malignant lymphoma, 2 mesothelioma of pericardium, 2 malignant myxoma, 1 angiosarcoma, 1 leiomyosarcoma, 1 fibrosarcoma and 1 rhabdomyosarcoma. Another 4 cases were not studied histopathologically. The clinical manifestations, ECG and X-ray findings of the 11 primary tumors were nonspecific but echocardiography was helpful to the diagnosis. Six patients were operated on and 1 died during hospitalization.

Effect of Astragulas membranaceus on natural killer cell activity and induction of alpha- and gamma-interferon in patients with Coxsackie B viral myocarditis.

The patients suffering from Coxsackie B viral myocarditis with depressed natural killer (NK) activity were treated with Astragulas membranaceus (AM) intramuscularly for 3-4 months. After the treatment, the NK activity was increased significantly from 11.5 +/- 11.9% before therapy to 44.9 +/- 15.0%. Another 6 patients of Coxsackie B viral myocarditis with depressed NK activity were treated with conventional therapy. The NK activity remained unchanged in 12.9 +/- 6%. The general condition and symptoms improved in all patients with AM therapy, while the titers of neutralizing antibody remained at the same level. Two days after AM treatment, the mean titers of alpha- and gamma-interferon (IFN) markedly increased in comparison with those before therapy and 3 weeks after AM therapy in 16 patients with Coxsackie B viral myocarditis, with left ventricular ejection fraction (LVEF) less than 65% and/or weak ventricular wall motion assayed by radionuclide angiocardiography. Whereas, in 12 patients treated with conventional therapy, there was no statistical difference among the results before and 2 days and 3 weeks after treatment. The results indicate that AM could partly regulate the lost of control of cellular immunity in patients with viral myocarditis.

Treatment of experimental Coxsackie B-3 viral myocarditis with Astragalus membranaceus in mice.

A murine model system for observing the effect of Astragalus Membranaceus (AM) on experimental myocarditis caused by Coxsackie B-3 virus (CB3V) was developed in 4-week-old male BALB/C mice. Gross, histopathologic and ultrastructural examinations of the infected-AM treated group showed that the severity and involved area of the myocardial lesions became milder and smaller than those in the infected-NS treated mice. The total lesion area, and the total lesion area/total myocardial area examined (%) and virus titer in the former group were also smaller and lower than those in the latter group. The results suggest that AM is effective in the inhibition of Coxsackie B virus propagation and protection of myocardium in mouse myocarditis.

[Effect of dexamethasone on Coxsackie B-2 virus-infected rat beating heart cells in culture].

The effects of dexamethasone (Dex) on cultured rat beating heart cells infected with 100 TCID-50 Coxsackie virus B-2 (CB2V) were observed. The beating % began to decrease in the infected group 2 or 3 d post-challenge. Meanwhile, the cytopathic effect (CPE) appeared rapidly from 1+ to 3+. In the infected and Dex-treated group 1 h after inoculation, the beating % and CPE in the whole flask were significantly higher and less, respectively, than that in the group infected (P less than 0.05) at the same intervals. At 5 d after challenge, the beating % in the whole flask was significantly higher than that in the infected group. The cardiac enzyme-aspartate aminotransferase (AST) in the infected group was higher than that in the infected and Dex-treated group (P less than 0.01) through 3-5 d post-challenge. Moreover, the AST levels in these 2 groups were also higher than that in the uninfected group, Dex control group at the same intervals (P less than 0.01). Ultrastructural findings were parallel to the results of CPE through 1-5 d post-challenge in these 4 groups. It is suggested that the protective effect of Dex on cultured beating heart cells infected with CB2V occurred in the early stages after infection. It is surmised that steroids can probably save the lives of patients with severe myocarditis if the conventional therapy for protecting the myocardium and improving immunity were administered together.

Reappearance of persistent normal sinus rhythm in a patient with the sick sinus syndrome following cardiac pacing for 10.5 years.

A patient with symptomatic sick sinus syndrome which manifested as a brady-tachy syndrome, was admitted to our institute in 1969. Following cardiac pacing for 10.5 years, the brady-tachy syndrome disappeared and normal sinus rhythm was restored. Her stable normal sinus rate has persisted up to the present, 2.5 years after termination of pacing.