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Plasma concentrations of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor type 1 (PAI-1), and D-dimer were investigated in 50 patients treated intravenously for acute myocardial infarction with either streptokinase (n = 23), urokinase (n = 17), or recombinant t-PA (rt-PA, n = 10). The fibrinolytic variables were measured by enzyme immunoassay on admission; 1, 2, 4, 6, 8, 12, and 24 h later; and then daily until day 7 after admission. In each subgroup of patients treated with different thrombolytic agents, PAI-1 increased significantly (P0.01) approximately 3 h after cessation of thrombolytic therapy. PAI-1 peak concentrations did not differ significantly (P = 0.82) among these three subgroups. t-PA and D-dimer did not differ significantly (P0.14) among subgroups except for higher t-PA in the rt-PA group attributable to detection of the therapeutically administered exogenous rt-PA by the t-PA assay. Our findings demonstrate a marked PAI-1 increase after thrombolytic therapy for acute myocardial infarction, which seems to be a common, drug-independent antifibrinolytic rebound phenomenon in response to thrombolytic treatment.

Cardiac troponin I, creatine kinase, and creatine kinase MB activity were tested in serial blood samples from 15 patients with first-time Q wave acute myocardial infarction (2 anterior and 13 inferior wall infarctions). All patients received intravenous thrombolytic therapy. Cardiac troponin I and creatine kinase MB activity were compared with scintigraphic estimates of myocardial scar (single photon emission computed tomography [SPECT] with 99mTechnetium-isonitrile [Tc-sestamibi]) on late images at rest about 5 weeks after myocardial infarction. Scintigraphic defect sizes ranged from 3.2 to 41.2% (median: 27.3%) of left ventricle. Cardiac troponin I increased and peaked in parallel with creatine kinase MB activity, and the peak values correlated with each other (r = 0.76, p = 0.002). Troponin I stayed increased for several days longer than creatine kinase and creatine kinase MB activity. It could be detected at least until the 4th day after admission. Significant correlation coefficients were found between 99mTc-isonitrile defect sizes and areas under cardiac troponin I curves (r = 0.53, p = 0.042) and between 99mTc-isonitrile defect sizes and cumulative creatine kinase MB activity release (r = 0.64, p = 0.01). Animal studies have already shown a very close correlation between histologic infarct size and SPECT 99mTc-isonitrile defect size. Therefore, our results indicate that cardiac troponin I release in patients with acute myocardial infarction is also correlated with infarct size.

Accurate diagnosis of impending acute myocardial infarction (AMI) in patients presenting at an emergency department with acute chest pain is essential for proper triage and treatment. We have developed an algorithm for the early diagnosis of AMI.The diagnostic performances of ECG, creatine kinase (CK) and creatine kinase isoenzyme MB (CKMB) activities, CKMB mass, myoglobin, and cardiac troponin T (cTnT) were compared for early diagnosis of AMI in 60 non-traumatic chest pain patients (22 AMI, 29 unstable angina, nine other diseases) on presentation to an internal medicine emergency department and 1 h thereafter. The classification and regression trees method was used for data analysis and revealed the following results.In patients with electrocardographic signs of acute transmural myocardial ischaemia on admission (mostly regional ST-segment elevations), biochemical markers could not improve the diagnostic accuracy either on admission or 1 h later. By contrast, in patients with non-diagnostic ECG, CKMB mass concentration measured 1h after admission was the best discriminator between AMI and non-AMI patients (discriminator value 5.8 micrograms/l) and was superior to ECG and all other biochemical markers tested. This algorithm for diagnosing AMI is characterized by 96% sensitivity, 90% specificity, 84% positive predictive value, 97% negative predictive value, 92% accuracy, 0.05 negative likelihood ratio, and 9.1 positive likelihood ratio.The classification procedure obtained allows accurate rapid and early diagnosis of AMI and could therefore be a valuable diagnostic aid to physicians of emergency medicine.

As a result of the limited sensitivity and specificity of creatine kinase and lactate dehydrogenase (LDH) as well as their isoenzymes, there is increasing interest in the use of cardiac contractile proteins for the diagnosis of acute myocardial infarction (AMI) and myocardial damage.This study compared the release of creatine kinase, creatine kinase MB, myoglobin, cardiac troponin I (cTnI), cardiac troponin T (cTnT), cardiac myosin light chain-1 (cMLC-1), and beta-type myosin heavy chains (bMHC) in serial blood samples from 13 patients (10 men, three women; median age 54 years, range 40-74 years) with first-time AMI (11 Q-wave, two non-Q-wave AMI; three anterior and 10 inferior wall AMI). All but one patient received intravenous thrombolytic treatment.Myoglobin was the first marker to increase in blood after AMI and showed the earliest peak levels, whereas bMHC increased latest, showing the latest peak levels. cTnI and cTnT increased significantly earlier than cMLC-1 and bMHC. cTnI and cTnT increased and reached peak levels parallel to each other, but the latter tended to stay increased longer. cTnT time courses were biphasic in the majority of AMI patients, unlike cTnI time courses. cMLC-1 release was mostly biphasic. cMLC-1 allows diagnosis during the acute phase as well as several days after the onset of AMI. The time courses of bMHC were usually monophasic. Its delayed appearance makes it useful for the diagnosis of remote infarction. In contrast to cTnI and cTnT, cMLC-1 and bMHC time courses were not significantly influenced by early reperfusion.Our results demonstrate the impact of the intracellular compartmentation of an intramyocardial protein (cytosolic, structurally bound, or structurally bound with soluble pool) on its concentration time course after AMI, particularly on the rapidity of its release.

Plasma concentrations of polymorphonuclear granulocytes elastase (PMN elastase) in complex with alpha-1 proteinase inhibitor are a marker of neutrophil activation. The latter complex, creatine kinase and cardiac troponin T, were measured in peripheral venous blood samples serially drawn in 39 patients with acute myocardial infarction. Of the total, 29 received intravenous thrombolytic therapy either with streptokinase (n = 15), urokinase (n = 7) or recombinant tissue type plasminogen activator (n = 7). Creatine kinase activities and cardiac troponin T concentrations were used as markers of myocardial tissue injury. In all patients with acute myocardial infarction, PMN elastase was elevated (median 80 micrograms/l, interquartile range 71 to 100 micrograms/l). Peak and cumulative (area under curve) concentrations of PMN elastase did not correlate closely with determinants of myocardial injury (r0.2, n.s.). PMN elastase increased during the first 6 h after starting thrombolytic therapy, whereas it decreased in conventionally treated patients and 12 h later increased. Maximum concentrations of PMN elastase, however, were not significantly higher in patients with thrombolytic therapy than in those without. In acute myocardial infarction patients with complications such as cardiac arrest with subsequent resuscitation (n = 5), cardiac rupture (n = 1) or cardiogenic shock (n = 2), PMN elastase plasma concentrations were significantly higher (p = 0.04) than in uncomplicated infarctions. In the complicated patients, changes in elastase concentrations paralleled or even preceded changes in the clinical presentation. Therefore, thrombolytic treatment seems not to significantly influence the amount of systemic neutrophil activation, but plasma PMN elastase could be a useful marker to monitor and identify complications in acute myocardial infarction.

Endothelin-1 concentrations were measured in peripheral venous blood samples from 42 patients with acute myocardial infarction. In patients with ischemic or hemodynamic complications (n = l1), endothelin-1 concentrations were significantly higher already on admission (P = 0.008) and remained significantly higher until day 6 after admission compared to patients with uncomplicated infarctions (n = 31; P = 0.035). There were no close correlations between peak concentrations of endothelin-1 and creatine kinase or creatine kinase isoenzyme MB mass in either group. Only in complicated patients did left ventricular ejection fraction correlate closely and inversely with peak endothelin-1 concentrations (r = −0.71; P = 0.03). Therefore, plasma endothelin-1 concentrations in patients with acute myocardial infarction patients may reflect states of markedly depressed cardiac performance and recurrent myocardial ischemia.

We investigated atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) in patients undergoing elective direct current cardioversion (CV group) due to atrial fibrillation (n = 9) or atrial flutter (n = 3). Anesthesia for cardioversion (CV) was induced with propofol 1.5 mg/kg. Conversion was achieved in all patients. Before CV all patients had elevated ANP and cGMP plasma levels. After CV the concentrations of ANP and cGMP decreased significantly within 15 and 30 minutes (p less than 0.01), respectively. Only one patient in the CV group showed increasing ANP and cGMP levels although his heart rate had decreased after CV and his blood pressure remained stable. High concentrations of ANP and cGMP might possibly be a compensatory mechanism of cardiac dysfunction. To study the influence the anesthetic agent on plasma levels of ANP and cGMP, we investigated six patients anesthetized with propofol for high-density radiation (HDR group). The data from this control group showed that propofol did not influence the plasma levels of ANP and cGMP. ANP correlated statistically significantly (p less than 0.05) with cGMP in both groups (r = 0.88 and 0.76 in the HDR and CV groups, respectively). In addition, we found a cGMP release of 149.6 +/- 17.6 per mol ANP in the HDR group, in the CV group the release was 109 +/- 54.2 cGMP per mol ANP. This phenomenon could be due to minor response of target cells to ANP stimulation (receptor down-regulation) in patients with heart disease. In conclusion, ANP and cGMP levels decreased after successful cardioversion.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaesthesia for elective direct current cardioversion (DCC) was induced with propofol (Diprivan) 1.2 mg/kg in 28 patients and with 0.2 mg/kg etomidate (Hypnomidate) in 20 patients. These mostly high risk patients (NYHA class II to III) were successfully treated with defibrillation. Blood pressure and heart rate were recorded before and after induction and at 2 minutes intervals up to 20 minutes after DCC. Both anaesthetic agents caused mild hypotension. Heart rate did not change significantly after induction but fell significantly after DCC from the mean value of 124 +/- 26 bpm and 122 +/- 37 bpm to 94 +/- 19 bpm and to 91 +/- 19 bpm in propofol and etomidate treated patients respectively. Four patients became apnoeic necessitating assisted ventilation for approximately four minutes. All propofol treated patients had rapid recovery times and opened eyes on command within 5.6 +/- 1.9 minutes after induction, and were fully orientated about 4 minutes later also. Complete amnesia was observed in all patients in this group. In contrast etomidate induced anaesthesia did not cause respiratory depression, but the recovery time was longer. Four patients of this group complained of recall of DCC. In 7 patients due to involuntary movements or myoclonus, after induction with etomidate reliable EKG monitoring appeared to be difficult.

In a multicenter, parallel, double-blind study, lisinopril was compared with atenolol in the treatment of mild to moderate essential hypertension. Four hundred ninety patients were randomized to a once-a-day treatment with lisinopril 20 mg or atenolol 50 mg for 4 weeks, and the doses of lisinopril or atenolol were increased up to 80 mg or 200 mg, respectively, at 4-week intervals if sitting diastolic blood pressure (SDBP) was not well controlled. Hydrochlorothiazide (HCTZ) 12.5 or 25 mg was added after 12 weeks, if necessary, and titrated upward after 4 weeks to a maximum dose of 25 or 50 mg/day. Lisinopril and atenolol reduced SDBP to a similar extent. All reductions from baseline in sitting diastolic and systolic blood pressure were significant (less than 0.01). Lisinopril produced a significant (less than 0.01) greater reduction in sitting systolic blood pressure (SSBP) than atenolol. Addition of HCTZ caused further blood pressure reductions (p less than 0.01). Five patients (1.7%) on lisinopril and four (2.0%) on atenolol developed skin rashes during weeks 1-12. Two patients (0.7%) on lisinopril 80 mg developed proteinuria (greater than 1 g/day). Cough occurred more often with lisinopril (4.5%), and elevated triglycerides occurred more often with atenolol (2.0%).

The effect of 0.5 mg Ouabain (O) i.v. on sinus node function and on intracardiac conduction was studied by His bundle electrography and atrial stimulation. 7 patients with normal sinus node function and av conduction (group I), 5 patients with sick sinus syndrome (group II), and 5 patients with av block of changing degree (group III) were examined. 2 additional patients had simultaneous sinus node dysfunction and av block (group II/III). The sinus node recovery time was prolonged in 6 patients, the av block was located proximal to the His bundle in 4 patients and distal to the His bundle in 3 patients. The spontaneous sinus rate decreased in group I and remained unchanged in group II and III after O. The PA interval increased slightly after O in groups II and III, the AH interval during sinus rhythm was prolonged after O in groups II and III and in the whole group together. During atrial pacing, the stimulus-His-time was increased in each group when compared at identical stimulation rates. In 4 of 7 patients av block type Wenckebach appeared at a lower stilmulation rate after O. The HV interval remained unaltered after O, the sinus node recovery time varied after O. Phenytoin had no positive effect on the changes observed after O. Unwanted actions of O such as increased bradycardia or increased av conduction disturbances were not observed. O appears to be reasonably safe in most patients with sick-sinus syndrome and changing av block.

106 episodes of ventricular fibrillation were observed in 11 patients, 9 of whom had acute myocardial infarctions. The heart rate before the onset of ventricular fibrillation was below 50 in two episodes, 60 to 100 in 63, and above 100 in 41. 83 attacks of ventricular fibrillation were preceded by fewer than five ventricular premature beats, 23 by more than five, 19 by more than ten. Multifocal ventricular premature beats occurred ten times, runs of ventricular premature beats 11 times, with only three falling into the vulnerable period. Left bundle branch block was present in three patients, right bundle branch block with left anterior hemiblock in two, isolated left anterior hemiblock in two, left posterior hemiblock in one. 85 episodes of ventricular fibrillation occurred during antiarrhythmic treatment, 72 during lidocaine administration. Antiarrhythmic drugs were effective only in reducing the number of ventricular premature beats. The only successful treatment of recurrent episodes of ventricular fibrillation was repeated electrical countershocks.

The purpose of the study was to evaluate the effects of nitroglycerin on the mechanical and metabolic performance of the mammalian heart without interference from peripheral vascular and neurohumoral influences. Isolated rat hearts were perfused with a buffer containing 1 mug of alcoholic nitroglycerin/ml or an equivalent amount of alcohol. Mechanical performance was analyzed during external and isovolumic work; all hearts were subjected to mild hypoxia. Heart rate was kept constant by pacing. At constant atrial filling pressures end diastolic pressures and calculated wall stiffness were not significantly different for controls and nitroglycerin. Afterload, as quantitated by mean aortic pressure, was the same for both groups. Peak-systolic left ventricular pressure and dp/dt max during ejection and isovolumic work were significantly reduced by hypoxia (p less than 0.001), but not changed by nitroglycerin. Cardiac output, mean systolic left ventricular pressure, work, oxygen consumption, and calculated efficiency were decreased by hypoxia (p less than 0.001); lactate production was enhanced by the hypoxic state (p less than 0.001). Nitroglycerin had no influence on these parameters in either state. It is concluded that at constant rate, preload and afterload nitroglycerin has no effect on the mechanical performance and energy formation by aerobic and anaerobic means in the fully oxygenated and mild hypoxic state.

The serum level of the myocardial-specific isoenzyme of creatine phosphokinase, CK-MB was determined in 50 patients with severe multiple injuries or following extensive surgery. It is concluded that whenever the proportion of CK-MB exceeds 10% of the total creatine phosphokinase activity myocardial damage has occurred, especially since equivalent ECG changes were registered in this group of patients.

This paper reports the case of a 55-year-old patient with complete obstruction of the aorta between the left common carotid artery and the left subclavian artery. The arterial blood supply to the lower half of the body is provided by extensive collateral networks in the region of the right hemithorax, the neck and the base of the brain. Only 10 similar cases appear to have been described in the literature; our patient seems to be the oldest so far.

The effect of an intravenous bolus of 1 mg/kg Ro 11-1781, a new calciumantagonist, on sinus node automaticity and intracardiac conduction was studied by His-bundle electrography and atrial stimulation. During sinus rhythm, no significant action of Ro 11-1781 on rate, P-A-interval, A-H interval, and H-V-interval was observed. The sinus node recovery time remained unaltered. On atrial stimulation, the St-H-interval was significantly (p less than 0.001) prolonged after Ro 11-1781. Wenckebach Periods occurred at lower stimulation rates in all patients after Ro 11-1781. It is concluded that Ro 11-1781 prolongs av nodal conduction and may be of therapeutic value in the treatment of supraventricular arrhythmias.

In 1971 a population-based Ischaemic Heart Disease (IHD) Register was established in the Innsbruck area as part of the WHO international collaborative study. Demographic and geographic data covering the area, as well as the locally-applied methods are described. One hundred and seventy four cases (133 males and 41 females) of acute myocardial infarction (AMI) were registered in the age group 20-64 years. This corresponds to an annual incidence rate of 1.9(0/00) in men and 0.6(0/00) in women. These results confirm indications from the national mortality statistics that Innsbruck belongs to the group of areas in Europe with a relatively low incidence of AMI. The epidemiology of AMI in Europe is discussed. The frequency distribution of AMI according to month of the year, day of the week and hour of the day is reported for this area.

In patients in coma due to severe CNS depressant drug overdose the central somatosensory conduction time (CCT) after median nerve stimulation is prolonged and N20 is dispersed. Brain-stem auditory evoked potentials demonstrate delayed interpeak latencies (IPLs) I-III, III-V and I-V. This was observed in 4 out of 5 patients investigated after intake of an overdose of amitriptyline (2 cases), barbiturates, meprobamate and nitrazepam (one case each). Toxic levels of drug overdose were related to prolonged CCT and IPLs, whereas normal CCT and IPLs were found at therapeutic drug plasma levels. CCT, IPLs and dispersion of N20 decreased during the course of coma. All patients were successfully treated. It appeared that SSEP and BAEP investigations could make a distinction between a 'toxic' and a 'therapeutic' coma level in severe drug overdose. It further appeared that normalization of CCT and IPLs preceded clinical improvement.

In the course of one year 357 patients were treated in our department for poisoning, nearly always with suicidal intent. Altogether 249 patients were admitted to the wards for 24 hours or longer, and 108 of these (44.6%) were taken into the intensive care unit. Apart from myocardial infarction (276 patients/year), poisoning is the most common reason for admission to the intensive care unit. The age distribution showed a maximum between 15 and 20 years. Only one case proved fatal, representing a mortality rate of 0.3%.

It has been suggested that the thromboischemic reentry mechanism (TRM) is responsible for washing platelet aggregates out of the coronary vessels during the early phase of acute myocardial infarction (AMI). This might account for the observation of Schwartz, who reported the presence of multiple microthrombi in the subendocardial blood vessels following AMI but found only a few thrombotic occlusions in the main coronary arteries. This washing-out of the vessel (due to reperfusion waves) intermittently releases myoglobin into the serum and is responsible for the "staccato phenomenon." We examined a group of 177 patients with a mean age of 66.1 years, whose sudden death was definitely of cardiac origin. Infarction was confirmed in 84.7% of the subjects (fresh infarct: 23.7%; fresh infarct with scarring: 25.9%; scarring alone: 35.0%; no change in myocardium: 15.2%). In other words, 49.7% of all postmortem subjects (88 cases) showed fresh infarction. Opening the coronary arteries longitudinally revealed only 7 thrombi in these 88 cases, i.e., 7.9% of all fresh infarcts. These observations confirm those of Roberts (8.5%) and Friedmann (4%).

Professional or spare time contacts with electrical appliances are, due to careless handling or technical inadequacies, potentially always associated with electrical injuries. The effects of the electric current on the body depends mainly on voltages: skin and muscle lesions predominate in high voltage injuries. Out of 23 patients, 19 with electrical injuries and 4 with lightning accidents, 18 showed normal ECGs at the time of hospital admission. There were no changes at follow-up. The remaining 5 patients had cardiac arrhythmias which disappeared after 1 1/2 to 36 hours using bedrest and symptomatic treatment only. Cardiac longterm monitoring is thus not required after electrical injuries.