Fibrinopeptide a (FPA) in patients with acute myocardial infarction.
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Biomedical subjects
Publications and source records attributed to E Orinius.
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A patient is described with ventricular tachycardia and premature beats (VPB) probably initiated by a diastolic wave, which--like the VPBs--could be eliminated by lignocaine and isoprenaline.
Thirty-eight non-operated patients with hypertrophic obstructive cardiomyopathy (HOCM) were followed for 1--18 years (mean 8). Twelve patients died, nine of them instantaneously without any other apparent cause of death. The symptoms on the first admission did not discriminate between those who died and those who survived during the observation period, nor did the findings at heart catheterization at rest or left ventricular angiocardiography. However, cardiac enlargement on the first chest X-ray was significantly more common in the decreased group, 75% against 27%, as was the complete absence of a q-wave in lead III on the first ECG, 83% against 42%. The combination of complete lack of q in lead III and cardiac enlargement on chest X-ray at the initial examination was present in 9 of the 12 deceased (75%) and in only 3 of 24 survivors (13%). This can be used to select patients for long-term prophylaxis against ventricular fibrillation which, according to the literature, is the main mechanism of instantaneous death in HOCM.
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The rectal temperature course was studied retrospectively in 192 consecutive patients with acute myocardial infarction (AMI). The ordinary temperature course after AMI was characterized by four points: 1. The morning temperature on the first day in hospital was seldom above 38.2 degrees C. (in four of 50 cases) 2. The maximal morning temperature was seldom recorded before day two or after day five in hospital (in five of 150 cases) 3. The maximal morning temperature seldom reached above 39.0 degrees C. (in one of 150 cases) 4. The morning temperature seldom increased more than 0.6 degrees C. after day five in one or more steps (in nine of 150 cases). Seventy-four per cent of the patients were afebrile after one week, and 96% after two weeks. Patients with higher SGOT (ASAT) maxima had longer duration of fever. Eleven per cent of the patients did not have fever at all.
Onset of atrial tachycardia, flutter or fibrillation occurred in 11% of 274 consecutive patients with acute myocardial infarction (AMI). Atrial tachycardia started about 24 hours and atrial flutter/fibrillation about 72 hours after onset of AMI symptoms. Left heart failure, diagnosed as pulmonary rales or frank pulmonary edema, was not more common in these patients before onset of tachyarrhythmias than among the rest of the patients. On the other hand, a notching of the P wave in lead CR-was significantly more common in the patients with atrial fibrillation (67%). In most of these cases the terminal P force in lead CR1 was not negative as in so-called left atrial enlargement. These findings suggest that atrial conduction disturbances might be a basis of atrial fibrillation in AMI.
In a consecutive series of 274 AMI cases ventricular tachycardia (VT), defined as three or more ventricular premature beats (VPBs) in succession but not VPBs, has been used as the indication for ventricular fibrillation (VF) prophylaxis. No primary VF occurred, and this fits with the hypothesis of VT as a sufficient indication for prophylaxis against primary VF. Six patients developed complicating VF (preceded by rales or hypotension but not frank pulmonary edema or shock). Four of the six patients (67%) had VT (0-1.5 hours) before VF, while the mean VT incidence of the six corresponding monitoring periods in 247 non-VF patients was 5%. Three of the four VT patients were on lignocaine/procainamide when VF developed. Thus, VT is acceptable as the only warning arrhythmia even in complicating VF but antiarrhythmic drugs do not seem to have the same prophylactic efficacy in complicating VF as in primary VF. Another 21 patients developed VF during shock, frank pulmonary edema or manipulating a pacemaker catheter within the heart.
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Diazepam has been used to an increasing extent in cardioversion, since avoiding general anaesthesia simplifier the procedure. The present study concerns the effect of diazepam on BP and blood gases in 13 cases of cardioversion. A moderate fall of both systolic and diastolic BP occurred. The arterial pO2 and pCO2 did not change significantly.
Serial estimations of total serum creatine phosphokinase (CPK) have been performed before and during 18-49 hours after submaximal physical exercise in 17 untrained individuals, mean age 50 years. The maximal CPK increase after exercise was 32 mU/ml (73%). The serum CPK did not exceed the upper normal limit (130 mU/ml) except in one individual (150 mU/ml). The maximal CPK increase in patients with acute myocardial infarction (AMI) varied between 101 mU/ml (133%) and 2 260mU/ml(3 790%), mean 900 mU/ml (1 184%). As the maximal CPK elevation in AMI occurs within the same period, it seems that heavy physical work of short duration just before the onset of symptoms will very seldom impair the diagnosis of AMI with the CPK technique used.
Serial estimations of total serum creatine phosphokinase (CPK) have been performed before and during 18-51 hours after cardioversion of supraventricular tachyarrhythmias in 12 patients without acute myocardial infarction (AMI). The maximal CPK rise was 78 mU/ml (110%) and the CPK did not exceed the upper normal limit (130 mU/ml) in more than two patients (149 respectively 156 mU/ml). The CPK rise we have observed in a series of AMI patients varied between 101 (133%) and 2 260 mU/ml (3 780%), mean 900 mU/ml (1 184%). Therefore, cardioversion performed as described seldom seems to interfere with diagnosing AMI by serial estimations of serum CPK during the next 24 hours.
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