[A comparative study in Stockholm. Significant differences between hospitals in mortality among patients with acute myocardial infarction].
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Biomedical subjects
Publications and source records attributed to N Rehnqvist.
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To assess the clinical usefulness of continuous on-line vectorcardiography (VCG), we studied 61 patients admitted to the coronary care unit (CCU) with chest pain, supposedly ischemic. Continuous VCG was performed for 24 h, monitoring QRS vector difference (QRS-VD), ST-change vector magnitude (STC-VM) and ST vector magnitude (ST-VM) measured 20 and 60 ms after the termination of the QRS complex. The patients were divided into four groups based on the final diagnosis; group A, 15 patients with normal exercise tests and extracardiac causes of chest pain; group B, 15 patients with unstable angina; group C, 15 patients with non-Q-wave myocardial infarction (MI); group D, 16 patients with Q-wave MI. Treatment was given according to a normal routine. Of 31 patients with MI, 16 received treatment with streptokinase. Groups A and B showed no significant permanent changes in QRS-VD, STC-VM or ST-VM. However, group B showed a higher occurrence of transient episodes (duration: 2 min-6 h) of a significant change of QRS-VD by > 15 microVs and of STC-VM, ST-VM 20 and ST-VM 60 by > 0.1 mV. Groups C and D showed both permanent changes and transient episodes for the studied vector parameters. Transient episodes were significantly fewer in group D than in group B. In patients with MI, the permanent change of vector parameters evolved more rapidly and reached a plateau earlier in those treated with streptokinase (QRS-VD: 178 +/- 82 vs. 293 +/- 100 min, p < 0.001; ST-VM 20: 142 +/- 75 vs. 293 +/- 89 min, p < 0.005). The magnitude of the end value for QRS-VD correlated with infarct size estimated by the maximal value of creatine kinase (r = 0.89; p < 0.001). We conclude that in patients admitted to the CCU with chest pain, continuous VCG monitoring early differentiates patients suffering from ischemic heart disease (IHD) from patients without IHD. It also differentiates patients with unstable angina from patients with MI.
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Beta-adrenoreceptor blocking agents have been used to relieve symptoms mainly in patients with ischemic heart disease. Prophylactic use of beta blockade in patients after acute myocardial infarction has shown a reduction in total mortality and also in sudden death. The overall total mortality reduction amounts to about 30%, whereas the reduction in the sudden death rate is 50%. The mechanisms behind this reduction in sudden death are probably manifold. Antiarrhythmic effects in ischemic myocardium, prevention of new ischemia, and also perhaps other factors may play a role. Apart from the prevention effect in chronic ischemic heart disease, beta blockers have also been able to reduce the sudden death rate in the long QT syndrome and are suggested for use in congestive cardiomyopathy.
Three defibrillators, one manual and two different semiautomatic, were prospectively compared during a one year period for out-of-hospital use by ordinary ambulance personnel with short additional training. Eighty-three cardiac arrest patients were treated with one of two different semiautomatic defibrillators and 26 by an ordinary manual defibrillator. Twenty-nine were found in ventricular fibrillation. Five of these patients were successfully resuscitated and admitted for further hospital care, two survived to be discharged home. The semiautomatic defibrillators were found to be accurate in ECG interpretation, sensitivity and specificity was 100%, respectively, and both were equally effective in defibrillation. There were no differences in conversion rate or in the clinical outcome between the three defibrillators tested. Both semiautomatic defibrillators tested seemed to be safe, reliable and cost-effective. The low survival rate found is most certainly due to a long ambulance delay.
Effects of in-hospital resuscitations performed by a trained resuscitation team were studied over a 20-month period during which 1653 deaths were registered. Resuscitative attempts were made in 61 patients with a mean age of 71 years (range 0-86 years). The underlying disease was ischaemic heart disease in 38 cases and most arrests occurred in general wards. Twenty-one patients were initially resuscitated; 12, however, died after an average of 3.2 days while still in hospital. Nine patients were discharged and seven are still alive after two and a half years.
We have studied 773 consecutive cases (706 individuals) with definite myocardial infarction treated in the Coronary Care Unit at Danderyd Hospital in Stockholm during the period 1984-85. Hospital mortality was 12.9% in all patients and 8.9% in patients under 70 years of age. Six hundred and six patients were discharged from the hospital and followed up for 2 years. The 2-year mortality in ischaemic heart disease was 14.4% in all patients and 9.5% in patients under 70 years of age and, including all causes of death, 20.3% and 14.6%, respectively. Our policy for medical treatment included frequent use of beta-adrenergic blocking agents, even in heart failure, and restricted use of antiarrhythmic drugs and digitalis. A short delay of admission may have been beneficial for the result of different kinds of anti-ischaemic intervention. Furthermore, a routinely performed exercise ECG before discharge and after 6 weeks, as part of a structured follow-up, has improved our ability to detect complications at an early stage and to optimize medical treatment.
In the patient with coronary artery disease, complex ventricular arrhythmias and frequent ventricular arrhythmias appear to be independent risk factors for subsequent death, particularly in patients who have had myocardial infarction. In patients with symptomatic arrhythmias, treatment must be instituted and tested during rigorous supervision of the patient. Using both the noninvasive Holter monitoring/exercise test procedure and invasive electrophysiologic testing, a beneficial antiarrhythmic response after institution of antiarrhythmic agents indicates improved prognosis. However, a negative treatment response during programmed stimulation does not necessarily indicate bad prognosis. This is particularly true for testing during amiodarone treatment. For unselected patients, routine antiarrhythmic treatment cannot currently be recommended. Continuing studies will show whether screening for electrical instability of the myocardium, and institution of antiarrhythmic therapy thereafter, will improve overall survival. If patients tolerate beta-blocking treatment, this should probably be instituted because reductions in mortality have been found, particularly in high-risk patients.
Heart failure is almost without exception associated with arrhythmias, which may be either supraventricular or ventricular. Supraventricular arrhythmias include frequent supraventricular extrasystoles, and episodic or chronic atrial fibrillation. The absence of atrial contraction may further reduce cardiac output, as may impaired control of QRS frequency. Therefore, supraventricular arrhythmias may be markers of the degree of heart failure and these arrhythmias will respond to heart failure therapy including diuretics, nitrates and, possibly, angiotensin-converting enzyme (ACE) inhibitors. Ventricular rate will be controlled by cardiac glycosides and further rate reduction obtained by verapamil or diltiazem. The rationale for this therapy is to optimize heart rate without compromising contractility. Severe heart failure is generally accompanied by severe ventricular arrhythmias including repetitive forms. Improving left ventricular function by ACE inhibition is accompanied by a reduction in the number of ventricular premature complexes and also a reduction in the rate of ventricular tachycardia. ACE inhibition reduces mortality but does not seem to influence sudden death rate, and sudden death patients may have different neurohormonal responses compared with patients destined to die of progressive heart failure. Uncontrolled trials with class IA or class III antiarrhythmic drugs have suggested that prognosis may be improved, but other studies have pointed out the increased risk of proarrhythmic responses in patients with low ejection fraction.
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The appropriate energy requirement for defibrillation of out-of-hospital ventricular fibrillation has been a matter of discussion. We analysed the effects of 360 J, 200 J or a combination of 200 and 360 J DC shocks given by ordinary manual defibrillators or semiautomatic defibrillators. 120 of 127 ventricular fibrillation episodes were converted by three or less 360 J DC shocks delivered by a manual defibrillator. All 28 ventricular fibrillation episodes were converted by an average of 1.9 DC shocks when 360 J were delivered by a semiautomatic defibrillator. 139 of 152 ventricular fibrillation episodes were converted by three or fewer 200 J DC shocks and 52 of 53 by 2 x 200 J followed, if needed, by 1 x 360 J DC shock delivered by the same semiautomatic defibrillator. Three or fewer 360 J DC shocks seems completely adequate for conversion of most episodes of out-of-hospital ventricular fibrillation. There is no difference in the result of defibrillation by manual and semiautomatic defibrillators.
The effects of resuscitation on patients who died suddenly out of hospital were evaluated after the introduction of early defibrillation performed by ambulance personnel using semi-automatic defibrillators. Resuscitation attempts were initiated in 548 patients during the 1-year study period. Mean ambulance delay was 7.5 min, 22% of the cardiac arrest patients had received bystander cardiopulmonary resuscitation (CPR). Sensitivity and specificity for the semi-automatic defibrillator in the interpretation of ventricular fibrillation was found to be 97 and 100% respectively. Only 28 (14%) of the 206 defibrillated patients regained circulation and were admitted for further hospital care. Only three survived to be discharged. Among the 342 patients in whom defibrillation was not indicated, 16 (5%) regained circulation and were admitted for further hospital care and one (0.3%) survived to be discharged. Semi-automatic defibrillators seem reliable, safe and inexpensive; however, the isolated addition of defibrillation to basal ambulance service seems to be inadequate in Stockholm. We need to evaluate what further resources are of importance to guarantee a successful outcome.
Long-term ECG recording on tape (LTER) was performed in 32 consecutive patients undergoing cholecystectomy. Twenty-two of the patients recorded showed ST-segment changes during the per- and early post-operative period. ST-segment depression was the most common change seen in 17 patients; however, 12 patients showed ST-segment elevation. In only nine patients were the ST-segment changes seen to be associated with major changes in pulse or blood pressure. ST-segment changes were seen as frequently in patients with, as without, known cardiovascular disease. All patients had an uncomplicated postoperative course and no case of myocardial infarction was seen. ST-segment changes during elective surgery seem to be a common phenomenon. The etiology of the observed changes is not clear and its value in the detection of per- or postoperative myocardial ischemia needs to be further evaluated.
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The effect of therapy on exercise performance during a 3-year follow-up after acute myocardial infarction (AMI) was evaluated in a double-blind randomized comparison between 154 patients given metoprolol (100 mg twice daily) and 147 patients given placebo. Exercise tests were performed 1.5, 6, 12, 24 and 36 months after AMI. Maximal accomplished workloads were similar in the 2 groups throughout follow-up. Maximal heart rate was significantly higher in the placebo-treated group throughout the study (p less than 0.001). At the 6-week test more patients in the placebo group terminated exercise due to angina pectoris (40 vs 25%, p less than 0.05) and showed exercise-induced ST-depressions (38 vs 27%, p = 0.05) compared with the metoprolol group. Exercise-induced ventricular arrhythmias were significantly more common in the placebo group during the initial 6 months. Death, another AMI or both were significantly reduced by metoprolol treatment in patients with exercise-induced ST depression greater than or equal to 1 mm at the 6-week test. In a multiple logistic regression analysis maximal accomplished workload at 6 weeks (p less than 0.026), male sex (relative risk [rr] = 3.57, p = 0.016), previous AMI (rr = 3.07, p = 0.001), therapy with placebo (rr = 2.14, p = 0.007) and left ventricular failure (rr = 2.04, p = 0.023) were shown to carry independent prognostic information as well as exercise-induced ST-depression (greater than or equal to 1 mm) in placebo-treated patients (rr = 2.70, p = 0.01).
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In a single-blind study of 6 weeks' duration, 32 patients with stable angina pectoris, who had been receiving controlled-release, Durules, isosorbide-5-mononitrate (Imdur) 60 to 180 mg daily for at least 1 year, were assessed after abrupt withdrawal of the nitrate. After 2 weeks of placebo treatment nitrate therapy was re-instituted, and the patients followed for another 2 weeks. The possibility of development of tolerance and rebound phenomena was also investigated. Three patients experienced severe anginal symptoms necessitating hospitalization when controlled-release isosorbide-5-mononitrate was withdrawn abruptly. Patients complained of more severe anginal symptoms during the placebo period, experienced more frequent anginal attacks and used more glyceryl trinitrate tablets than during active treatment. ST segment changes during exercise were more pronounced with placebo. After controlled-release isosorbide-5-mononitrate was re-introduced, these variables indicated significant improvement. On the other hand, no deterioration occurred in exercise performance during the placebo phase. Responsiveness to glyceryl trinitrate was maintained, as shown by comparisons of exercise tests performed after the long term treatment and during the placebo phase. Controlled-release isosorbide-5-mononitrate retains a beneficial effect in patients with angina pectoris during prolonged use, although some attenuation of the effect is seen. Abrupt withdrawal of the drug is not recommended because of the possibility of severe exacerbation of anginal symptoms, although no clearcut rebound phenomena were seen.