The delay between the onset of symptoms and the call for help is the longest single component of the time taken for patients with acute myocardial infarction to come under coronary care and receive thrombolytic therapy. In order to investigate factors influencing patient delay, visual analogue scores for pain, shortness of breath, and anxiety were obtained retrospectively from 250 patients with acute myocardial infarction, for the time of onset of symptoms, and for the time of the call for help. The predominant symptom was chest pain, followed by anxiety and breathlessness. Although all symptoms increased in severity after their onset, the initiation of a call was largely unexplained in terms of worsening symptoms. Patient delay had a skewed distribution with modal, median and mean values of up to 1 h, 1.5 h, and 11 h respectively. Patient delay was negatively correlated with the pain score at the time of calling, but most of the variance of patient delay could not be explained in terms of symptom scores. However, patient delay was independently and negatively related to maximum serum aspartate aminotransferase. During acute myocardial infarction, patients with higher cardiac enzyme levels experience more pain and delay less. This tendency for patients with more severe infarction and a greater risk of death to call for help sooner is an added reason for administering thrombolytic treatment at the first opportunity: those patients who call early have most to gain from prompt therapy.
In a retrospective 6 year follow up data were obtained for 536 of 566 (95%) consecutive patients admitted to a coronary care unit with acute chest pain. Their diagnoses were acute myocardial infarction in 290 (54%), myocardial ischaemia in 164 (31%), pericarditis in 16 (3%), and non-cardiac in 66 (12%). Six year mortality was 36%, 24%, 0%, and 16% respectively. In patients with acute myocardial infarction a higher mortality rate during follow up was associated with a higher than average age, a higher than average creatine kinase, previous myocardial infarction, Q wave infarction, and the presence of reciprocal changes. The presence of reciprocal changes was associated with higher than average concentration of serum creatine kinase, indicating more extensive infarction. Infarction complicated by ventricular fibrillation or left bundle branch block was associated with a higher death rate.The electrocardiogram recorded at the time of acute myocardial infarction contains much useful prognostic information. To investigate these points we studied a consecutive series of patients presenting to a coronary care unit with acute chest pain who were followed up over a six year period. Patients and methodsOver a one year period 566 consecutive patients presented to a coronary care unit with acute onset of chest pain. Follow up data were obtained for 536 (95%), who are the subjects of this report. Their mean age was 55 years (range 24-78 years); 399 were male and 137 were female. Details of the electrocardiogram on presentation and of any subsequent ehanges or arrhythmias during the hospital stay were recorded, together with personal details and past medical history. The patients were followed up retrospectively by reference to their hospital case notes or by contact with their general practitioners. Details of subsequent cardiovascular events and the cause of death were obtained wherever possible.The diagnosis of acute myocardial infarction was made if two ofthe following were present: a characteristic history of more than 30 minutes chest pain, a rise in the concentration of serum creatine kinase of > 75 U/l, and the development of characteristic echocardiographic changes. All the electrocardiograms were recorded in 12 lead format at a paper speed of 25 mm/s and 10 mm/mV.We used the following definitions: Q wave myocardial infarction. The development of abnormal Q waves in at least two adjacent infarct related leads.Non-Q wave myocardial infarct. Important ST segment change or T wave inversion in at least two adjacent inferior leads or three adjacent anterior leads not progressing to the formation of abnormal Q waves, with these changes persisting for at least 24 hours."Enzymatic infarction". Acute chest pain with an abnormal rise of creatine kinase to at least twice the upper limit of normal but no significant electrocardiographic changes.Reciprocal changes. ST segment depression > 1 mm at or after 0-08 s from the J point of the QRS complex in leads VI-V3 in inferior infarcts and leads 2, 3, and aVF in anterior ...
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