Cardiac gammagraphy with technetium 99 pyrophosphate in myocardial infarct

The predominant fatty acids (C10-C18) of dermatophytes were investigated by the Landsteiner-Draize test to establish their allergenicity. It was demonstrated that fatty acids can give rise to sensitization of delayed type in guinea pigs. The middle-chain fatty acids (C10-C12) showed a high allergenicity compared to the (C13-C18) acids with moderate to weak contact sensitizing properties. The fatty acids may act as contact sensitizers and, at least sometimes, be responsible for the skin lesions in dermatophytosis.     

Serum levels of cardiac troponin I and troponin T in estimating myocardial infarct size soon after reperfusion

BACKGROUND: Cardiac troponin I (TnI) and troponin T (TnT) are highly specific myocardial markers. OBJECTIVE: To determine whether their serum levels can be used to estimate myocardial infarct size soon after reperfusion. METHODS: We measured the serum levels of TnI, TnT, and creatine kinase every 3 h, and the serum cardiac myosin light chain I (MLCI) every 24 h, in 42 patients with acute myocardial infarction in whom reperfusion therapy had successfully been performed. We calculated the severity of regional hypokinesis by analyzing the follow-up ventriculograms with the centerline method. RESULTS: The time from reperfusion to the peak level for TnI was 6.1 +/- 3.5 h, significantly shorter than those for creatine kinase (7.5 +/- 4.1 h) and MLCI (55 +/- 28 h). The time to peak level for TnT (6.8 +/- 4.0 h) differed significantly from that for MLCI but not from that for creatine kinase. There was a significant correlation between the peak levels of TnI and TnT (r = 0.86). The peak TnI and TnT levels were correlated well to the peak creatine kinase level (r = 0.67 and 0.69, respectively), total creatine kinase release (r = 0.66 and 0.66), and the peak MLCI level (r = 0.71 and 0.80). We observed excellent correlations between the peak levels of TnI and TnT, and regional hypokinesis (r = -0.84 and -0.85, respectively). These were comparable to the correlations between regional hypokinesis and the peak creatine kinase level (r = 0.75), total creatine kinase release (r = -0.72), and the peak MLCI level (r = -0.76). CONCLUSIONS: These results suggest that the peak serum levels of TnI and TnT in patients with successful reperfusion are accurate and early indices of infarct size.     

High-resolution electrocardiography in acute myocardial infarct

The author starts by highlighting the importance of risk stratification in patients who have survived a myocardial infarction. High resolution electrocardiography, also called signal-averaged electrocardiography (SAECG), appears in this setting as a diagnostic tool that, by providing important information about the way the intraventricular conduction of the electrical impulse is made, contributes to the characterization of the arrhythmogenic substrate, which is the basis of ventricular tachycardia and fibrillation. By resorting to the averaging of the electrocardiographic signal, SAECG enables us to detect ventricular late potentials whenever the analysis of that signal is made in time-domain. Further details, which will enrich the information on ventricular activation, can be obtained if the analysis is made in the frequency-domain (spectral analysis). The importance of detecting abnormalities in the SAECG recordings lies in the fact that those abnormalities are related to the occurrence of ventricular tachycardia and fibrillation, which are responsible for arrhythmic death. After referring to the criteria of positivity of SAECG and its reproducibility, the author approaches the most important part of the paper: the clinical applications of SAECG. After focusing on the interest of the method in noncoronary conditions, its usefulness in patients with acute myocardial infarction is pointed out. The author then mentions the prevalence of abnormalities in SAECG in patients with acute myocardial infarction and emphasizes the interest of the method in risk stratification. The author then presents the results of his Group in what concerns prevalence and prognosis. Finally, the author refers to the application of SAECG in other forms of coronary artery disease besides myocardial infarction.     

Nutritional problems in acute myocardial infarct

Hypocaloric nutrition in patients during the first days of myocardial infarction cannot be suggested any longer. Because of several reasons the minimum calory uptake should be about 2000 kcal/per day. Patients with enddiastolic pulmonary artery pressures above 20 mm Hg which is especially a high risk group should be treated parenterally with solutions of carbohydrates, insulin, and potassium. This regimen appears to be of a special importance at beginning shock or during cardiogenic shock.     

The apexcardiogram in acute myocardial infarct

The relation between intracardial haemodynamics and apicocardiogram (ACG) parameters is explained. A wave (amplitude and duration), A/H ratio, true and total TCI, total systole, total expulsion, RIV, RFW, TE/TCI (total) and TE/TCI (true) findings in 22 patients with acute myocardial infarct are presented. Attention is also given to clinical and radiological signs of cardiac insufficiency and the infarct site. Constant and significant increases in the A wave, A/H ratio and RIV, together with a decrease in total expulsion, were noted, particularly in cases with clinical evident insufficiency. In the pre-expulsive stage, ACG Data could not be taken as a reliable index of myocardial contractility in cases where insufficiency was not manifest. It is felt, therefore, that ACG may be of assistance in the evaluation of changes in myocardial performance, even where clinical and radiological signs of decompensation are absent.     

Biochemical markers in acute myocardial infarct

Exact and early diagnosis of acute myocardial infarction is essential for the subsequent routine management of this frequent cardiovascular disease. At present, the clinical biochemistry possesses a set of more or less cardiospecific protein markers for early detection of myocardial ischemic damage. After the admission of patient to the hospital, serial estimations of rather non-specific enzyme activities (creatine kinase, its MB-izoenzyme, lactate dehydrogenase, hydroxybutyrate dehydrogenase) are currently used for the detection of acute myocardial infarction and for the further monitoring of the patient and managing his therapy. In the past decade, many cardiospecific biochemical markers were discovered and gradually introduced into the routine clinical practice. The most perspective markers are some molecules of contractile proteins of heart myofibrils (troponins, myosin chains) as well as "rediscovered" myoglobin. The aim of this review article is to inform about the commonly used, as well as about the new biochemical markers, to discuss some problems of diagnostic strategy in the early and exact detection of ischemic myocardial damage and to attract attention to the difficulties. However its disadvantage resides in its presence in both myocardium and skeletal muscles which arise when the diagnosis of acute myocardial infarction is prematurely excluded from consideration and such patients are discharged too soon from hospital. (Fig. 1, Tab. 1, Ref. 72.)     

Ventricular arrhythmias and sudden cardiac death in acute myocardial infarct in the era of thrombolytics

Sudden cardiac death (SCD) in the setting of acute myocardial infarction (AMI) remains an actual problem. There is a very close relationship between ventricular arrhythmias and SCD in AMI. Malignant ventricular arrhythmias, such as ventricular fibrillation and ventricular tachycardia are the major causes of SCD in coincidence with AMI. Frequent and complex ventricular arrhythmias are also important predictors of the risk of SCD in coincidence with and after AMI. In this article the authors emphasize the importance of the complexity of pathophysiological mechanisms responsible for the genesis of ventricular arrhythmias in coincidence with AMI. The necessity of taking into account the current knowledge about pathophysiology in prevention and therapy of separate forms of ventricular arrhythmias is also emphasized. The incidence and time course of ventricular arrhythmias and SCD in coincidence with AIM in prethrombolytic and thrombolytic periods is described. The importance of separate forms of ventricular arrhythmias in coincidence with AMI with regard to short and long-term prognoses is described. There are discussed also the possible mechanisms of thrombolytic and adjuvant therapies that affect the incidence and frequency of ventricular arrhythmias. The authors recommend the optimal therapy for each form of ventricular arrhythmia and the following management of patients with AMI. In the prevention and therapy of ventricular arrhythmias in the setting of AMI the authors emphasize the importance of early recanalization and prevention of re-occlusion of the infarction-related coronary artery. Great importance is attributed also to other adjuvant measures directed to the restriction of the size of infarction, myocardium protection, prevention and attenuation of remodelling of the left ventricle and thereby to the prevention of heart failure and attenuation of adverse effects of the sympathetic nervous system. An early administration of beta-blockers which favourable effect in and after AMI was documented with conclusive evidence is considered as one of the most important measures in prevention and therapy of malignant ventricular arrhythmias and SCD. The occurrence of malignant ventricular arrhythmias in the setting of heart failure and/or 24-48 hours after AMI should be an indication for aggressive management directed to arrhythmia (programmed ventricular stimulation, electrophysiologically guided pharmacologic or nonpharmacologic therapy) as well as to underlying coronary heart disease (coronary angiography and revascularization).     

The pre-hospitalization period in acute myocardial infarct

The article reviews the possibilities of biochemical markers in coincidence with the assessment of prognosis in acute coronary syndromes and in the revealing of effectivity of their therapy. The current options of clinical biochemistry in many cases allow to supplement, confirm, or exclude the results of modern physical and other clinical examination methods and in this way to contribute to the accuracy of the diagnostic process, and enable to comment the prognosis and the risk measure of the patient. A significant progress has been achieved in the assessment of effectivity in thrombolytic therapy in acute myocardial infarction, where especially the series assessment of myoglobin levels or specific troponin cardiomarkers can facilitate the process of physician's decision as to the assessment of the subsequent procedure in the treatment of patients. The assessment of levels of both specific and partly less specific cardiomarkers becomes one of the criteria of the decision in coincidence with ischaemic episodes in the peri and postoperative periods (the diagnosis of peri-operative myocardial infarction). Specific troponin cardiomarkers acquire an extraordinary significance in the prediction of the measure of risk in patients with unstable angina pectoris where already one single assessment of the level of these markers is sufficient for hospitalization of the patient and thus enables to change the physician's strategy of further therapy. (Ref. 95.).     

Angina in the acute phase of myocardial infarct

Factor VIII (AHG) activity was assayed in the plasma specimens from 1016 regular and controlled blood donors. Age and ABO blood groups had highly significant effects on factor VIII concentrations, whereas the effect of sex was not significant. The median in the donors of blood group O rose from 87% at the age of 20 to 119% at the age of 60 years, and the median in blood groups A and B+AB of corresponding ages rose from 108 to 147%. An interaction effect of age and blood groups was present only at the 5% level of significance. The present data and the previous findings of others suggest the existence of an association between high factor VIII levels and thrombotic states.     

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.)     

Treatment acute myocardial infarct in the pre-hospital phase

OBJECTIVE: To examine the circadian variation in the signal averaged electrocardiogram (saECG) and heart rate variability and investigate their relations in healthy subjects. METHODS: 24 hour ECGs were obtained with a three channel recorder using bipolar X, Y, and Z leads in 20 healthy subjects. The following variables were determined hourly: heart rate, filtered QRS (f-QRS) duration, low and high frequency components of heart rate variability (LF and HF), and the LF/HF ratio. RESULTS: Heart rate, f-QRS duration, HF, and the LF/HF ratio showed significant circadian rhythms, as determined by the single cosinor method. Heart rate and the LF/HF ratio increased during daytime, and f-QRS duration and HF increased at night. f-QRS duration was negatively correlated with heart rate (r = 0.95, p < 0.001) and the LF/HF ratio (r = 0.94, p < 0.001) and positively with HF (r = 0.93, p < 0.001). CONCLUSIONS: f-QRS duration has a significant circadian rhythm in healthy subjects and is closely related to the circadian rhythm of autonomic tone.     

A paradigm shift for acute myocardial infarction: from coronary patency to myocardial reperfusion

OBJECTIVE: To evaluate the safety and efficacy of amitriptyline hydrochloride in the treatment of severe recurrent idiopathic cystitis (IC) in cats. DESIGN: Prospective study. ANIMALS: 15 cats with IC that failed to respond to other treatments. PROCEDURE: Each cat received 10 mg of amitriptyline, PO, every 24 hours in the evening for 12 months or until signs recurred. Urinalysis, CBC, serum biochemical analysis, urine bacteriologic culture, and cystoscopy were performed initially, and after 6 and 12 months in responders. Severity scores of owner-observed signs of lower urinary tract (bladder and urethra) disease were recorded. RESULTS: During the first 6 months of treatment, 11 of the 15 cats had no owner-observed signs of lower urinary tract disease. During the next 6 months, 9 of 15 cats remained free of signs of cystitis. Despite clinical improvement, cystoscopic abnormalities persisted in all cats at the 6- and 12-month evaluations. Hematuria and proteinuria were decreased at the 12-month evaluation compared with the initial evaluation. Two of 15 cats initially appeared somnolent after amitriptyline treatment. Of 9 cats completing the study, 7 had increased body weight and 8 had decreased coat quality compared with the initial evaluations. Four cats developed small cystic calculi during the first 6 months of the study. Serum biochemical or hematologic abnormalities were not detected during the study. CLINICAL IMPLICATIONS: Amitriptyline treatment successfully decreased clinical signs of severe recurrent IC in 9 of 15 cats treated. Somnolence, weight gain, decreased grooming, and transient cystic calculi were observed during treatment in some cats.     

Salivary PAF in acute myocardial infarction and angina: changes during hospital treatment and relationship to cardiac enzymes

Salivary levels of platelet activating factor (PAF) were measured together with serum CPK and interleukin 2 receptor in 30 patients admitted to the coronary care unit, 9 patients with pulmonary tuberculosis, 10 with acute severe asthma and 8 normal controls. 16 of the 30 C.C.U. patients had sustained a acute myocardial infarction (M.I.) 5 had acute angina and the remaining 9 had non cardiac chest pain. Salivary PAF on admission was significantly higher in the M.I. Patients than in the normal subjects, asthmatics, tuberculosis patients and those with non cardiac chest pain (p < 0.001 in all cases) but not those with angina. After 48 hours PAF levels fell in the subjects with M.I. (p < 0.01) and no significant difference was seen between any group. PAF levels did not show any relationship with CPK levels or site of infarct in the M.I. patients. Interleukin 2 receptor was not significantly raised in the M.I. group as a whole but some individual patients showed markedly increased serum levels, but these levels did not correlate with either salivary PAF or serum CPK.