Adjuvant therapy in patients with acute myocardial infarct

Besides the thrombolytic therapy several adjuvant therapeutic measures were identified which significantly improve the prognosis of patients with acute myocardial infarction (AMI). These measures include the treatment by means of acetylsalicylic acid (ASA), beta-blockers and ACE inhibitors. Early administration of ASA and beta-blockers are indicated in all patients with AMI who have no contraindications for this therapy. They are especially the patients with manifest heart failure or asymptomatic left ventricular dysfunction who benefit from ACE inhibitors. The effectivity of routine administration of other medicaments such as anticoagulants, nitrates, calcium channel blockers and magnesium, have not been convincingly proved. However, some selected patients with AMI can benefit from these medicaments. Intravenous administration of heparin is unambiguously justified only in thrombolysis with t-PA. Thrombolyses with streptokinase, urokinase, and anistreplase are justified only at high risk of thromboembolic complications. Their prevention and therapy include also the necessity to restrict the administration of pelentan. The use of nitrates is indicated in patients with AMI in case of sustaining stenocardia, arterial hypertension and manifest heart left ventricular failure. Until the definitive standpoint is gained regarding the effect of magnesium in patients with AIM, its administration remains especially indicated in cases of arterial hypertension, tachycardiac disturbances of the heart rhythm and states of assumed or proved hypomagnesiemia. In AMI cases when magnesium is used in order to protect the patient from reperfusion lesion, it must be administered prior to the reperfusion therapy. An intensive research in the field of therapeutical measures in patients with AMI still continues. It is certain that it will soon bring further knowledge which will in turn improve the prognosis and quality of life of patients with AMI. (Tab. 4, Ref. 133.)     

Criteria for evaluating the effectiveness of myocardial infarct patient rehabilitation (posthospital phase)

On the basis of the analysis of a 24- to 30-month posthospital phase of rehabilitation in 486 patients with myocardial infarction, critera were elaborated for dividing them into 4 classes with mathematically determined severity index. Criteria for analysing rehabilitation efficacy available for wide practice and a definite algorithm for differentiated management of patients with stage by stage appraisal of the condition and reaching alternate decisions are suggested. The strict dependence of the results of the post-hospital rehabilitation phase on the appraisal of the patients, condition and the corresponding correction of the rehabilitation program is shown.     

Chlamydia pneumoniae infection in patients with myocardial infarct and angina pectoris

In a prospective open study we investigated Chlamydia pneumoniae infections in 36 consecutively admitted patients: 26 males, mean age 53.4 yr, range 36-70 yr, 10 females mean age 57.7 yr, range 47-70 yr, suffering myocardial infarction (24 acute, 2 previous) or angina pectoris (10). Antibody serum levels were measured by the immunefluorescent method and they were as follows: negative 5, low 12, medium/high 11, chronic infection 5, recent infection 3. The 3 cases considered as recent infections are described in detail.     

Hemodynamic studies of patients with recent myocardial infarct by means of radiocardiography

The effect of endotoxin to depress the hepatic drug-metabolizing enzyme activity has been studied in the C3H/HeJ and C3H/HeN strains of mice. The C3H/HeJ mouse strain is generally considered to be unresponsive to the biological effects of endotoxin. However, injection of these mice with 0.5 mg/kg body weight of E.coli endotoxin (Westphal extracted) produced a decrease in the rate of N-demethylation of ethylmorphine and in the levels of cytochrome P-450 and cytochrome b5 comparable to that observed in the endotoxin-sensitive C3H/HeJ mouse strain. Although the mechanism of endotoxin action to decrease hepatic microsomal drug-metabolizing activity is presently unknown, the results suggest that: 1) the C3H/HeJ mouse stain is responsive to this endotoxin effect, and 2)that cellular constituents other than B-cells or macrophages are probably involved in eliciting the response, since these cells of the C3H/HeJ mouse are unresponsive to endotoxin.     

The behavior of late potentials in myocardial infarct patients undergoing myocardial revascularization

A novel 30 kb deletion of the beta-globin gene cluster associated with the phenotype of hereditary persistence of fetal hemoglobin (HPFH) is described in two unrelated individuals of Vietnamese background. The Vietnamese G gamma A gamma HPFH deletion has a unique 5' breakpoint 3.5 kb downstream of the delta-globin gene. The 3' breakpoint lies approximately 8 kb upstream from the HPFH-3 breakpoint (Henthorn et al., 1986) and in the region of the 3' breakpoints of HPFH-4 (Saglio et al., 1986), German and Belgian G gamma+ (A gamma delta beta)zero-thalassemias (Anagnou et al., 1988; Losekoot et al., 1991). Characterisation of the 3' breakpoint in the present study has enabled more precise localisation of other deletion breakpoints at this locus. Further evidence is provided that the 3' breakpoint region contains functionally important sequences and that the juxtaposition of these sequences to the gamma-globin genes is a significant factor in the increased fetal hemoglobin levels.