N. Sammel

Prediction of serious arrhythmic events after myocardial infarction: Signal-averaged electrocardiogram, holter monitoring and radionuclide ventriculography

Noninvasive assessment was undertaken before hospital discharge in 210 patients who had recovered from acute myocardial infarction. This comprised signal-averaged electrocardiography, Holter monitoring and radionuclide left ventriculography. An abnormal signal-averaged electrocardiogram was defined as the presence of a low voltage signal less than 20 microV in the terminal 40 ms of the filtered QRS complex or a long filtered QRS complex greater than 120 ms. During a follow-up period of 6 months to 2 years (median 14 months), 15 patients had arrhythmic events: eight died suddenly and seven presented with sustained, symptomatic ventricular tachycardia. Using univariate analysis, abnormalities in each of the three noninvasive tests were able to predict arrhythmic events. Stepwise logistic regression demonstrated that each test was independently significant in predicting outcome, with a left ventricular ejection fraction less than 40% being the most powerful variable (beta = 2.8, p less than 0.005). This process generated an algorithm that allowed assessment of combinations of variables: the finding of an abnormal signal-averaged electrocardiogram in the presence of an ejection fraction less than 40% identified patients with a 34% probability of arrhythmic events. By contrast, in patients with left ventricular dysfunction but a normal signal-averaged tracing, the risk of arrhythmic events was 4% (p less than 0.001). This combination of variables was associated with a sensitivity of 80% and a specificity of 89%. Hence, using a combination of noninvasive tests after myocardial infarction, patients can be stratified according to risk of serious arrhythmic events.

PROTECTIVE EFFECT OF PROPRANOLOL IN THREATENED MYOCARDIAL INFARCTION

Propranolol 0.1 mg/kg intravenously followed by 320 mg orally over 27 h was given to 20 randomly selected patients within 4 h of the onset of suspected myocardial infarction unaccompanied by diagnostic electrocardiographic changes. Patients given propranolol had fewer completed infarcts as assessed by serial electrocardiograms, a lower frequency of serum-creatine-kinase levels above the normal range, and lower peak serum-creatine-kinase levels than 23 control subjects. This evidence suggests that threatened myocardial infarction can in some cases be prevented by early beta-adrenoceptor blockade.

Signal-averaged electrocardiogram for evaluation of recurrent syncope

Signal-averaged electrocardiography (ECG) was performed in 150 consecutive patients presenting with syncope, to determine its diagnostic role in identifying patients with ventricular tachycardia (VT) and in determining their long-term prognosis. Patients also underwent a standardized investigational protocol to independently determine a cause of syncope. Twenty-nine patients had a late potential, 107 had a normal signal-averaged electrocardiogram and 14 had bundle branch block on 12-lead ECG. Signal-averaged ECG identified a late potential in 16 of 22 patients with VT and was normal in 101 of 114 patients in whom syncope was attributed to causes other than VT or remained unexplained (sensitivity 73%, specificity 89%, predictive accuracy 55%). In patients with coronary artery disease, the predictive accuracy increased to 82%. Absence of a late potential identified a group of patients with a very low incidence of VT. During follow-up of 1 to 20 months (median 11), 15 patients (10%) died, 6 suddenly. There was no significant difference in survival or recurrence of syncope between patients with and without a late potential. Signal-averaged ECG can noninvasively identify patients with serious ventricular arrhythmias among an unselected group presenting with syncope.

Randomized controlled trial of intraaortic balloon counterpulsation in early myocardial infarction with acute heart failure

The value of intraaortic balloon counterpulsation in limiting infarct size and improving survival was studied in patients with early transmural myocardial infarction complicated by acute heart failure. Thirty such patients, previously well, were randomly assigned to counterpulsation (14 patients) or standard therapy (16 patients). Counterpulsation was begun 4.8 to 13.7 hours (mean 7.1) after the onset of pain and continued for less than 1 to 11 days (mean 4.5). Peak creatine kinase was 1,794 +/- 846 IU/liter (mean +/- standard deviation) in patients receiving counterpulsation compared with 1,688 +/- 908 for those receiving standard therapy; cumulative creatine kinase was 3,590 +/- 1,936 IU/liter for patients receiving counterpulsation and 2,945 +/- 1,803 for those receiving standard therapy. Hospital mortality was similar (counterpulsation, 7 of 14; standard therapy, 7 of 16 [p = 0.05 for 25 percent mortality reduction]) as was mortality at follow-up (counterpulsation, 8 of 14; standard therapy, 10 of 16 [p = 0.09 for 25 percent mortality reduction]). Functional class at follow-up examination 1 to 36 months (mean 15) after infarction was also similar in the two groups. Counterpulsation did not appear to modify infarct size or to alter morbidity or mortality when initiated as primary therapy 4.8 to 13.7 hours after the onset of symptoms of myocardial infarction.

Natural history of late potentials in the first ten days after acute myocardial infarction and relation to early ventricular arrhythmias

Serial signal-averaged electrocardiograms (ECGs) were performed every 48 hours in 50 patients admitted to the coronary care unit with acute myocardial infarction. The prevalence of late potentials was 32% at presentation (mean time to recording 12.4 +/- 6.6 hours after onset of chest pain) and increased progressively throughout the hospital stay. New late potentials were recorded in patients with no prior acute myocardial infarction as early as 3 hours after the onset of chest pain and as late as 8 days. Late potentials appeared transiently in only 3 patients. The detection of late potentials in the initial signal-averaged ECG identified patients with clinically significant early ventricular arrhythmias with a sensitivity of 80% and specificity of 72%. The predictive accuracy was 38% for a positive test and 94% for a negative test. Patients with early ventricular arrhythmias had significantly lower voltage in the terminal 40 ms of the filtered QRS complex (16 +/- 8 vs 32 +/- 19 microV, p less than 0.01) than those without arrhythmias. The signal-averaged ECG may be useful in identifying patients at high risk of developing clinically significant early ventricular arrhythmias after acute myocardial infarction.

Arterial counterpulsation in severe refractory heart failure complicating acute myocardial infarction.

The role of arterial counterpulsation was sought in 100 patients with severe refractory cardiac failure complicating myocardial infarction. Seventy-four were in shock and 26 were not. Average duration of counterpulsation was 7.0 days. Hospital survival was 34 per cent (25/74) in shock (predicted less than 10%) and 65 per cent in patients who were not in shock (predicted less than 50%). Survival at 4 years was 10 +/- 4 per cent in shock and 37 +/- 11 per cent in patients not in shock; functional status was class 1 or 2 in 5 of 9 patients in shock and in 8 of 12 survivors not in shock. Results were best when counterpulsation was started early after onset of symptoms, when ischaemic pain was still present, or when a mechanical defect was corrected surgically. Early coronary artery bypass surgery performed alone in 9 patients did not influence survival or functional status. Complications of counterpulsation occurred in 17 patients in shock and in 2 patients not in shock, all but 6 on the first day; none directly caused death. Counterpulsation is an effective and safe adjunct to medical treatment of complicated infarction provided the intervention is prompt.

A method for coronary artery calcium scoring using contrast-enhanced computed tomography

BACKGROUND Limitations to the coronary calcium score include its requirement for noncontrast imaging and radiation exposure that approaches current methods for contrast-enhanced CT angiography. OBJECTIVES We sought to derive and validate a method of measuring the coronary artery calcium score (CACS) from standard contrast-enhanced CT, obviating the need for a second non-contrast calcium scan. METHODS The volume of intramural calcium of >320 HU in major coronary vessels was measured in 90 contrast-enhanced and traditional non-contrast calcium scan pairs. An empiric conversion factor was derived to convert the small voxel contrast-enhanced calcium volume to an Agatston calcium score. The accuracy of this technique was then prospectively validated in 120 consecutive patients undergoing clinical calcium scans and contrasted-enhanced coronary CT. Eleven patients were excluded from analysis because of the prespecified criteria of excessive noise in the contrast-enhanced CT or total coronary artery occlusion. RESULTS The Pearson correlation of the contrast scan-derived calcium score with the measured CACS was r2 = 0.99. With standard CACS risk bands, agreement of the contrast-enhanced calcium score estimate with the measured CAC by quadratic weighted κ was 0.96. The 95% limits of agreement (Agatston units) were given by ±(3.2 + 0.14 × CACS + 4.44 mean square root of CACS). Inter-observer and intra-observer reliability with the intraclass correlation was 0.99. CONCLUSION The calcium score can be accurately measured from contrast-enhanced cardiac CT scans with the use of a Hounsfield unit threshold of 320.

Treatment of acute myocardial infarction with propranolol. Further studies on enzyme appearance and subsequent left ventricular function in treated and control patients with developing infarcts.

were used: (a) total creatine kinase appearance and peak activity levels measured during the acute stage of infarction, and (b) subjective analysis of biplane left ventriculograms performed one month later in a subgroup of these patients. Total enzyme appearance was reduced by 25 per cent and peak levels were reduced by 23 per cent in treated patients compared with controls. The subgroup subsequently studied by angiocardiography did not show the reduction in enzyme levels shown by the whole group; likewise, quantitative subjective analysis of the left ventriculograms did not show any significant difference between the two groups. Though it could not be confirmed by this radiological method that reduction in enzyme appearance by beta adrenoceptor blockade was associated with restriction in infarct size, this seems the most likely cause for the lower enzyme levels. The safety of intravenous beta blockade when used in carefully selected patients suggests that large-scale clinical trials can be recommended in which measurements of infarct size as well as morbidity and mortality can be used

Comparison of enzymic with cineangiocardiographic estimations of myocardial infarct size.

Comparisons were made between enzymic indices of myocardial infarct size (total creatine kinase appearance and peak enzyme activity) measured during the acute state of a first myocardial infarct in 32 male patients, and analysis of contraction abnormalities in biplane left ventricular cineangiocardiograms performed one month later. The cineangiocardiograms were analysed independently by two radiologists, each using two different methods for quantification of subjectively classified abnormalities of left ventricular wall motion. A very strong correlation was found between the two enzymic indices of infarct size and somewhat weaker correlations between assessment of contractility abnormalities made by the two radiologists using the same method, or by the same radiologist using the two different methods. Comparisons between enzymic and angiocardiographic indices for all infarcts showed correlation coefficients (r) within the range of 0.53 to 0.72. With all comparisons of enzymic with radiological indices r values were higher for anterior infarcts than for inferior infarcts, and there was a tendency for higher enzyme levels for a given degree of left ventricular damage in inferior than in anterior infarction. This may be the result of variable degrees of right ventricular damage in inferior infarction.

Prognostic implications of loss of late potentials following acute myocardial infarction.

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during seriai testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G‐week follow‐up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 ± 11 msec at discharge to 104 ± 11 msec (P < 0.01), terminal QRS voltage rose from 15 ± 4 μV to 31 ± 9 μV (P = 0.001), and late potential duration fell from 42 ± 6 msec to 28 ± 6 msec (P = 0.001) at the 6‐week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non‐Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6‐week assessment, 11 additional arrhythmic events occurred during median follow‐up of31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P ‐ NS) but significantly greater than palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal‐averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal‐averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.