Prevention of sudden cardiac death.
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Biomedical subjects
Publications and source records attributed to F G Dunn.
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To investigate the significance of the electrocardiographic (ECG) pattern of left ventricular hypertrophy and strain, two groups of asymptomatic patients with essential hypertension were compared. The patients were similar in terms of age, smoking habit, serum cholesterol and blood pressure levels, but differed in the presence (Group I, n = 23) or absence (Group II, n = 23) of the ECG pattern of left ventricular hypertrophy and strain. Group I patients had significantly more episodes of exercise-induced ST segment depression (14 versus 4, p less than 0.05) and reversible thallium perfusion abnormalities (11 of 23 versus 3 of 23, p less than 0.05) despite similar exercise capacity and absence of chest pain. Nonsustained ventricular tachycardia was detected on 24 h ambulatory ECG monitoring in two patients in Group I, but no patient in Group II. Coronary arteriography performed in 20 Group I patients demonstrated significant coronary artery disease in 8 patients. This study has shown that there is a subgroup of hypertensive patients with ECG left ventricular hypertrophy and strain who have covert coronary artery disease. This can be detected by thallium perfusion scintigraphy, and may contribute to the increased risk known to be associated with this ECG abnormality.
Because thrombolytic treatment is effective only if it is given within six hours of acute myocardial infarction it is vital to admit patients to the coronary care unit as soon as possible after the acute event. A policy of admitting patients to the coronary care unit at the request of the patient's general practitioner by a telephone line that is independent of the hospital switchboard significantly reduced the delay. Those admitted via the accident and emergency department at the same hospital reached the coronary care unit 1 h 32 min after being seen by the general practitioner whereas the patients admitted directly took only 43 minutes [corrected]. The policy of direct admission also significantly increased both the percentage of patients who received thrombolytic treatment and the percentage of patients admitted within three hours from the onset of symptoms.
The case reports of 186 intravenous drug abusers admitted over a three year period were studied. Nineteen had proven staphylococcal septicaemia. Echocardiography showed tricuspid vegetations in seven and aortic vegetations in two. Eighteen out of 19 had systolic murmurs, but only the two patients with aortic vegetations had diastolic murmurs. The chest x ray showed opacities in 10 patients (all those with tricuspid vegetations plus three with normal echocardiograms). Four patients died during follow up, including both those with aortic vegetations; both mitral and tricuspid vegetations were found at necropsy in the other two. All remaining patients were alive at one year. The presence of tricuspid vegetations in intravenous drug abusers is associated with opacities on chest x ray, but carries a good short term prognosis. But these results suggest a poor outcome when left sided endocarditis is present in intravenous drug abusers.
There is a need for a simple clinical measurement that will indicate the extent of myocardial salvage after successful thrombolysis. This study examined whether coronary artery reperfusion reduced the infarct size as assessed electrocardiographically after thrombolytic treatment. The sum of the (sigma) ST segment area in leads showing ST segment elevation in the 12 lead electrocardiogram at presentation was used as an index of potential myocardial injury (initial ischaemic index). The evolved infarct size at 48 h was assessed by a QRS scoring system. Two groups of patients, both admitted with anterior myocardial infarction within 6 h of onset, were studied. Group 1 (n = 35) received analgesia only and group 2 (n = 33) received thrombolytic treatment either by the intracoronary (streptokinase, n = 13) or intravenous route (anistreplase, n = 20). Reperfusion was assessed angiographically. The mean (SD) potential infarct size assessed by the initial ischaemic index was similar in both groups (group 1, sigma ST area = 115 (60) mm2 and group 2 = 126 (77 mm2). The QRS score representing evolved infarct size was significantly lower in the treated group (4.1 (2.5] than in group 1 (7.8 (2.6]. The 95% confidence intervals for QRS scores based on the admission sigma ST area from patients with successful reperfusion were applied to a third set of patients (n = 22) to test the ability of the admission ST area (myocardial injury) to predict the QRS score accurately. While patients with successful reperfusion had significantly lower QRS scores than those who did not (4.5 (3.1) versus 9.3 (3.4)), the wide confidence intervals caused by inter-individual variability precluded an accurate prediction of the QRS score in an individual from the sigma ST area at time of presentation. There was no difference in infarct size in patients treated early (</= 3 h) (QRS score 4.2(2.8)) or later (3-6 h) (4.1(2.1)). This study provides evidence that sequential electrocardiographic changes are reduced in patients with anterior infarction who achieve reperfusion after thrombolytic treatment and that this benefit is shown with treatment given up to six hours after infarct onset. None the less, the relation between the initial ischaemic index and the evolved QRS score has wide confidence intervals, reflecting inter-individual variability, and does not allow the prediction of a QRS score in an individual patient.
One hundred and eleven patients over the age of 65 years who underwent coronary artery bypass grafting in Glasgow between 1980 and 1985 were compared with 548 younger patients, who had coronary artery bypass surgery over a similar period of time. The elderly group had a higher prevalence of females, pre-operative unstable angina, left main coronary artery disease and depressed left ventricular function. There were no significant differences between the two groups in operative morbidity or mortality and angina was abolished or improved in 93% of the elderly patients at follow-up. Coronary artery surgery has an important role in the management of angina in elderly patients.
It has previously been suggested that amiodarone, used widely to treat refractory cardiac arrhythmias, may induce glucose intolerance. In view of this, we have undertaken a prospective study in a group of 10 patients with normal glucose tolerance profiles requiring amiodarone therapy for control of supraventricular or ventricular dysrhythmias. The patients were followed for a total of 9 months, and glucose tolerance tests and glycosylated haemoglobin were done at 3 monthly intervals in all patients. Both fasting blood glucose levels and glucose tolerance tests were entirely within normal limits in all patients at each stage during the study. Glycosylated haemoglobin did rise significantly at 6 months, but this did not exceed the normal range in the majority of patients and the rise was not sustained at 9 months. In this prospective study therefore, there is no evidence of either glucose intolerance or a diabetogenic effect during prolonged therapy with amiodarone.
The predictive value of the measurement of changes in ST segment elevation was assessed as a non-invasive marker of coronary artery reperfusion after thrombolytic treatment. Forty five patients with acute myocardial infarction (23 anterior, 22 inferior) of less than six hours' duration were given thrombolytic treatment by either the intravenous (n = 28) or the intracoronary route (n = 17). A proportional value for the shift in ST segment, termed the fractional change, was calculated both from 12 lead electrocardiograms and from the Holter tape for each patient. Coronary artery patency in an initial group of 22 patients (training group) was associated with a fractional change value of greater than or equal to 0.5 (100% specific, 88% sensitive by Holter analysis; 100% specific, 94% sensitive by 12 lead electrocardiogram). This rule performed well when it was applied to a test group of 17 patients (100% specific, 93% sensitive by Holter analysis; and 67% specific, 93% sensitive by 12 lead electrocardiogram). Linear discriminant analysis was then used to determine which features gave the best separation of those in whom there was reperfusion and those in whom there was not. This gave 100% specificity and 100% sensitivity when applied to the training group for either the 12 lead electrocardiogram or Holter monitoring. When it was applied to the test group, the sensitivity was maintained at 100%, but the specificity dropped to 33% irrespective of whether the basis of the test was Holter monitoring or the 12 lead electrocardiogram. These results suggest that a fractional change of >/= 0.5 calculated from a single lead showing myocardial injury is a useful non-invasive marker of reperfusion. The technique can be applied to either 12 lead electrocardiograms or Holter monitoring. The use of a more complex classification increased the sensitivity of the test at the expense of its specificity.
The electrocardiograms (ECGs) of a series of 34 patients with primary hyperaldosteronism (PHA), 17 treated surgically (group I) nine treated medically (group II) and eight treated with/by both surgery and drug therapy (group III) were analysed to determine whether the treatment of PHA resulted in an improvement in the ECG changes of left ventricular hypertrophy (LVH) and also whether there was a difference in this improvement between medically and surgically treated patients. There was a significant reduction of blood pressure in the group as a whole (186/111 to 141/95 mmHg, P less than 0.001) and within each of the treatment groups (group I 183/108 to 137/98 mmHg, group II 188/112 to 147/93 mmHg, group III 193/115 to 144/92 mmHg). This reduction within each group was of a similar magnitude. There were reductions in both precordial voltages (SV1 + RV5) from 3.68 mV to 2.79 mV (P less than 0.01) and in the number of patients with ECG LVH from 15 to 8 (P less than 0.05). Again the reductions were of similar magnitude in each of the groups: group I 3.78 to 2.77 mV, group II 3.78 to 2.84 mV, group III 3.39 to 2.77 mV. Thus the improvement in blood pressure achieved by the treatment of PHA is accompanied by a reduction in precordial voltages and the number of patients with ECG-LVH. This improvement is independent of the type of treatment used.
Considerable attention has properly been focused in recent years on electrocardiographic abnormalities in patients with essential hypertension. It has been well established that both voltage evidence of left ventricular (LV) hypertrophy and LV hypertrophy and strain are ominous risk factors. A better understanding of the strain pattern in patients with LV hypertrophy has arisen from experimental animal studies showing how an increase in cardiac mass can lead to myocardial ischemia and from clinical studies showing that the patient with LV hypertrophy and strain is at risk from myocardial ischemia as a consequence of both associated coronary artery disease and increased LV mass. All the clinical syndromes associated with myocardial ischemia are increased in patients with LV hypertrophy and therefore earlier recognition of both cardiac involvement and myocardial ischemia is likely to improve survival in this particularly high-risk group of patients.
Fifty-seven elderly patients (35 males, 22 females; age range 65-80 years, mean 70 years) with acute myocardial infarction received thrombolytic therapy within 8 h using either streptokinase or anisoylated plasminogen streptokinase activator complex. Coronary artery reperfusion was confirmed by early coronary arteriography. The overall reperfusion rate was 77%. Accurate non-invasive markers of reperfusion included: a rapid fall in the S-T segment elevation, an early peak of the creatinine phosphokinase enzyme curve and reperfusion arrhythmias. Clinical events suggesting early reocclusion occurred in 30%. Coronary arteriography was accompanied by local bleeding associated with the arterial puncture site in 2 patients and a cerebrovascular accident in 1 patient. Minor bleeding occurred in 6 other patients. In those where reperfusion occurred, the mortality at 1 month was 6.6% and in those who did not reperfuse or had early reocclusion 38%. At 1 year the figures were 10 and 46%, respectively.
Regression of left ventricular hypertrophy occurs with a number of antihypertensive drugs, but the time course of this regression has not been defined clearly. We obtained echocardiograms at baseline and serially (on seven occasions) during a 1 year treatment period with the beta-adrenergic receptor inhibitor atenolol in 12 patients with previously untreated essential hypertension. To ensure control of blood pressure in all patients throughout the study, it was necessary to add a thiazide diuretic to the therapy of five patients. Baseline blood pressure was 155/100 mm Hg and fell to 136/84 mm Hg; there was a 20% reduction in heart rate. Posterior and septal wall thicknesses were reduced from 1.16 +/- 0.03 to 1.06 +/- 0.02 cm (p less than .05) and from 1.28 +/- 0.07 to 1.18 +/- 0.06 cm (p less than .05), respectively; this reduction became significant initially at 4 weeks. Left ventricular mass decreased from 144 +/- 9 to 127 +/- 7 g/m2 (p less than .05) and this fall first became statistically significant at 6 months. Significant reduction in electrocardiographic voltages was also seen at 6 months. Therefore, regression of left ventricular hypertrophy with atenolol-induced blood pressure control occurred as early as 4 weeks after starting therapy and was maintained thereafter without apparent compromise of left ventricular systolic function.
Obstruction of a Bjork-Shiley mitral valve prosthesis occurred in a 41 year old woman due to pannus tissue growing over the valve and impairing disc opening. The unusual intermittent nature of the obstruction was clearly demonstrated by Doppler ultrasound. The pannus was excised and the valve prosthesis replaced successfully with a Carpentier-Edwards xenograft.
Anisoylated plasminogen streptokinase activator complex (APSAC) is a recently developed thrombolytic agent with high fibrin-binding potential and sustained release pharmacokinetics (plasma half-life 70 minutes). Following studies of its intracoronary use, the efficacy was examined, in an open study using coronary angiography, of a single bolus dose of 30U given intravenously to 94 patients within 6 hours (mean 2.97 hours) from the onset of symptoms of myocardial infarction. After thrombolytic therapy, patency of the left anterior descending artery was demonstrated in 32 of 42 patients with anterior infarctions (76%), and in 12 of 13 patients with circumflex (92%) and 28 of 36 with right coronary artery infarcts (78%) in the inferior infarction group. The overall incidence of reocclusion was 24%, which occurred within the first 12 days after hospitalisation. Successful thrombolysis was associated with rapid resolution of the acute ST segment change, and an early peak of creatine phosphokinase (CK) compared with patients whose vessels remained occluded. No major systemic bleeding complications were experienced. Single dose intravenous APSAC appears to be a highly effective and relatively safe thrombolytic agent which has the major advantage over other such agents of easier administration. This makes it suitable for use in district hospitals and in the community, as well as in specialised cardiac centres.
Arteriosclerotic heart disease is now the most important cause of morbidity and mortality in the elderly. Clinical presentation may be less typical than in younger patients, and therefore, a high index of suspicion is necessary. Although selectivity is required in regard to investigations, age should not deter the physician from establishing a diagnosis and quantifying the extent of the coronary artery disease. In this way, management will prove rewarding in terms of both symptomatic relief and prolonged survival with improved quality of life.
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In view of recent interest in the relationship of haematocrit and blood viscosity to hypertension and vascular disease, we have analysed retrospectively the relationship of haematocrit to blood pressure, vascular complications and other variables in 2,381 patients referred to the Glasgow Blood Pressure Clinic. Haematocrit correlated negatively with age and systolic pressure in men, and positively with age and systolic pressure in females. Positive correlations were found in both sexes between haematocrit and serum alanine aminotransferase (possibly due to mutual correlation with alcohol); and between haematocrit and overweight (Quetelet Index) but not obesity (Ponderal Index). Increased haematocrit was also associated with cigarette smoking; and with history of angina, myocardial infarction and intermittent claudication in females. No correlation was observed between haematocrit and history of stroke. These findings suggest that prospective studies of haematocrit in hypertensives may be of interest.