Biomedical subjects
Publications and source records attributed to D A Chamberlain.
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Despite the importance of early thrombolysis in the treatment of acute myocardial infarction, unacceptable delays in drug administration still occur in hospital. From March 1989 we decided to monitor our performance, and thereby to reduce avoidable in-hospital delay to a minimum. Potential candidates for thrombolytic therapy were identified by paramedic ambulancemen whenever this was feasible. Rapid check-lists were used for inclusion and exclusion criteria in the Accident and Emergency Department. A target of 15 min was set for time to treatment, and reasons for any gross deviation (greater than 30 min) were explored in each instance. As a result of these strategies, we achieved a median time from admission to initiation of thrombolysis in 50 consecutive patients of 17 min. The 39 patients treated with injections of APSAC as opposed to infusions of streptokinase had a median in-hospital delay to treatment of only 13 min.
Seven of 475 consecutive patients treated with thrombolysis for acute myocardial infarction had severe embolic complications that were believed to be caused by disintegration of pre-existing clot. Three patients had symptoms that persisted for many weeks, and five died. Any potential site of pre-existing blood clot within the vascular system, notably an enlarged left atrium, ventricular aneurysm, or aortic aneurysms, should be regarded as a contraindication to treatment with thrombolytic agents.
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Data available experimentally and from major trials suggest that the beneficial effects of thrombolysis depend on more than simple reperfusion. New knowledge regarding the dynamic nature of clot formation and clot lysis enables us to understand more of the processes involved in thrombolysis. The breakdown of systemic fibrinogen may be important because of the anticoagulant effect this can produce. Other beneficial effects of thrombolysis remain unproved or obscure. It is unlikely that any thrombolytic agent can be completely free of risk because no distinction is possible between a hemostatic plug and a pathologic thrombus. There may, however, be differences between agents in the likelihood of reocclusion. The value of active intervention with angioplasty or bypass grafting after thrombolysis remains undefined. Three major trials suggest that little erosion of initial benefit occurs over the first 12 months even when management is largely conservative. If thrombolysis leads to smaller infarct size, however, prognosis should be influenced favorably over a prolonged period. Parallel mortality curves between treated and placebo groups therefore suggest that some attrition is occurring to counteract what might otherwise be continuing prognostic benefit. The ideal thrombolytic agent should be inexpensive to manufacture, have a low risk of hemorrhagic complications, be nonallergenic, provide rapid and complete thrombolysis, have some anticoagulant properties, be easy to administer and suitable for readministration. However, a low risk of hemorrhage is probably incompatible with effective thrombolysis. A comparison of mortality results with the 3 existing agents are awaited with interest.
The evolution of surface ventricular late potential activity was studied in 50 patients during the 6 weeks after first acute myocardial infarction (AMI). In 15 of 47 patients (32%) late potential activity appeared within 6 hours of the onset of major symptoms. Its prevalence overall remained approximately 30% at each recording time but with marked individual variability in appearance. Late potential activity was associated with late ventricular arrhythmias (greater than 24 hours after AMI) but not with early ventricular arrhythmias (less than 24 hours after AMI). Late ventricular arrhythmias or sudden death occurred only in the 6 patients with late potential activity (p less than 0.05). Early ventricular fibrillation (15 patients) occurred equally in the patients with and without late potential activity. Thus, late potential activity occurs at some stage in the first 6 weeks after AMI in 50% of patients, but its timing is variable. It is a sensitive but not specific predictor of late ventricular arrhythmias and sudden death, but not of early ventricular fibrillation.
Do passenger deaths occur during commercial air travel? If so, how often and from what causes? We reviewed information reported to the International Air Transport Association on in-flight deaths that occurred during commercial air travel for the eight years between 1977 and 1984. Of the 120 airlines in the International Air Transport Association, 42 carriers reported deaths during these eight years. A total of 577 in-flight deaths were recorded, for a reported average of 72 deaths per year. Deaths occurred at average rates of 0.31 per million passengers, 125 per billion passenger-kilometers, and 25.1 per million departures. The majority of those who died were men (66%, 382/577) and middle-aged (mean age, 53.8 years). Most of the individuals (77%, 399/515) reported no health problems prior to travel. Physicians aboard the aircraft offered medical assistance for 43% (247/577) of the deaths. More than half of the deaths (56%, 326/577) seemed to be related to cardiac problems. Sudden unexpected cardiac death was the cause of death in 63% (253/399) of the apparently healthy people and seems to be the major cause of death during air travel. These observations support the initiation of programs to train cabin personnel in the skills of basic cardiopulmonary resuscitation and in the use of automatic external defibrillators.
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The role of combined alpha and beta blockade as a means of limiting infarct size has been studied in a randomised controlled trial using labetalol. Only 166 of 630 (26%) consecutive patients admitted to a cardiac care unit with suspected myocardial infarction were deemed suitable for inclusion; most of the remainder had delayed admission to hospital, were over the age limit of 75, or had complications which precluded the use of labetalol. Those on active treatment received a loading dose followed by a slow intravenous infusion over six hours, and oral therapy for the subsequent five days. Doses were adjusted to maintain systolic pressure in the range 100 to 120 mmHg. The control group received only conventional therapy. Labetalol caused lowering of the blood pressure and heart rate during the phase of intravenous treatment, but little effect occurred subsequently because oral dosage was constrained by low systolic pressures. The group that received active treatment had significantly greater release of CKMB enzyme. Little difference was observed in R wave scores or ejection fraction. Only low doses of labetalol can be used for most patients with acute myocardial infarction. Labetalol cannot be recommended as routine treatment for normotensive patients admitted to hospital with suspected infarction.
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The efficacy of transvenous cardioversion and defibrillation for treating life threatening spontaneous ventricular arrhythmias was assessed in a study of 17 patients in a cardiac care unit. Eleven had ventricular tachycardia, five had ventricular fibrillation, and one had both. Transvenous cardioversion successfully terminated tachyarrhythmias on 42 separate occasions in ten patients. Stable electrode positions could not be achieved in two patients, recurrent late displacement occurred in one, and four patients had no further arrhythmias requiring cardioversion once the lead was placed. The energy levels required for successful cardioversion ranged from 0.05 J to 25 J for ventricular tachycardia and from 1 J to 25 J for ventricular fibrillation. The nine successful shocks of 1 J or less did not require sedation or general anaesthesia. High energy (25 J) endocardial shocks were unsuccessful in terminating arrhythmias in two patients, one with ventricular tachycardia and the other with both ventricular tachycardia and fibrillation. Minor unwanted effects of endocardial shocks occurred in five patients. These were acceleration of ventricular tachycardia in two patients and complications of pacing via the special lead in three others: failure of sensing occurred in all three and one patient also had a transient rise in pacing threshold. A postmortem examination in one patient who had received three unsuccessful high energy shocks revealed localised endocardial necrosis at the site of the distal electrode. Transvenous cardioversion offers advantages over external cardioversion but at present practical difficulties limit its application to patients with recurrent ventricular arrhythmias that cannot readily be controlled by conventional methods.
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Progress in understanding the epidemiology and mechanism of sudden cardiac death (SCD) has been rapid over the past two decades. This, together with the availability of drugs with actions that potentially may counter the pathophysiology of sudden death, has led to myriad trials aimed at prolonging life for high-risk individuals. European countries have contributed a major share both to the development of these drugs and to subsequent tests of their efficacy. Ventricular fibrillation (VF), either unheralded or secondary to fresh myocardial ischemia, is by far the most common cause of SCD. The classes of drugs with profiles that might be expected to influence the occurrence of VF directly are antiarrhythmics, calcium channel blockers, platelet-active agents, and beta-adrenoceptor antagonists. Twenty-four of the European trials that employed agents from these groups have special significance because of their design and size. Studies of two of the calcium channel blockers have not demonstrated any life-saving potential to date. One platelet-active agent - aspirin - has shown favorable trends. Results with the use of antiarrhythmic agents have been disappointing, probably because their adverse effects, including arrhythmogenesis in some patients, have countered the antiarrhythmic effects that other patients have achieved. Nevertheless, evidence suggests that lidocaine can reduce the incidence of VF; this can reasonably be equated with life-saving potential whenever defibrillation is not available. Trials with beta-blocking drugs have been the most encouraging; seven of the 11 trials that have been considered demonstrated a significant reduction in sudden death, which was variously defined, and a strong trend toward reduction was observed with another. None of the trials showed an unfavorable trend. The results of completed trials now offer practical guidance to physicians with responsibility for the care of patients with ischemic heart disease, especially those who have features that indicate high risk.
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