Value of the electrocardiogram for prediction of left ventricular mural thrombus in anterior wall acute myocardial infarction.
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Biomedical subjects
Publications and source records attributed to B Strasberg.
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Ten patients, who were admitted to the Intensive Coronary Care Unit during a one year period with symptomatic bradycardia while on combination therapy with oral diltiazem and beta-blocker agents, are described. The important features of this adverse reaction to drug combination were that it appeared mainly in a relatively elderly age group and with presenting symptoms of lethargy, dizziness, syncope, chest pain, and (in one patient with poor left ventricular function) pulmonary edema. It was not dose dependent and occurred even in very low doses of each drug. Electrophysiologic abnormalities were localized to the sinus node in all 10 patients and the primary rhythm disorders were junctional escape rhythm, sinus bradycardia, and sinus pause. These rhythm abnormalities resolved within 24 h following withdrawal of the offending drugs. Temporary pacemaker insertion was necessary in four patients. The duration of drug combination used before the acute episode range from within hours to up to 2 years. In conclusion, although combination diltiazem/beta blocker therapy is very effective in ischemic syndrome, caution is advised when this combination is used especially in the elderly or in patients with left ventricular dysfunction or antecedent sinoatrial or atrioventricular conduction abnormality.
During three consecutive days of prazosin treatment in a patient with pheochromocytoma, urinary catecholamine metabolite levels were correlated with plasma renin activity. Suppression of renin plasma activity resulted in sustained hemodynamic and clinical improvement, while no remarkable changes were observed in urinary catecholamine metabolite levels. This suggests that prazosin may interrupt the vicious cycle of worsening hypertension provoked by further activation of the renin-angiotensin system mediated by excessive circulating catecholamines.
We present 2 cases in whom repetitive rapid ventricular tachycardia (VT) was the initial manifestation of metastatic cardiac disease. In one patient, repetitive VT appeared during chemotherapy for stage IV paratesticular rhabdomyosarcoma which led to the diagnosis of cardiac metastases. In the other, it led to the diagnosis of malignant pericardial effusion 17 years after successful therapy for a breast carcinoma. In conclusion, in patients with present or past history of malignancy, the appearance of life-threatening VT should raise the suspicion of cardiac metastases.
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Late potentials occur after the QRS complex and can be detected by using signal averaging and filtering techniques. In this study the filtered averaged electrocardiograms (ECGs) obtained using two types of filters were compared: the bidirectional digital recursive filter with a 40 Hz high-pass cut-off frequency, and the Fourier transform non-recursive digital filter with a 60 Hz high-pass cut-off. Strong correlation was found between the numerical values obtained when using these two filtering procedures. In addition, close diagnostic concordance was found between the late potential parameters in patients with normal and abnormal signal averaged ECGs. Visual comparison between the bidirectional and the Fourier plots revealed a close morphological similarity between the vector magnitudes. There was no significant difference in the mean root mean square voltage of the terminal 40 ms and the late potential duration, less than 40 mV, between the bidirectional and the Fourier filters in patients with a normal or an abnormal signal averaged ECG. The QRS duration was found to be significantly longer using Fourier filtering. This can be explained by the contributions of two factors: using the bidirectional procedure with a phase delay from each end of the data window, a shortening of the filtered QRS duration may occur and, alternatively, when using the Fourier filter, minimal stretching of the QRS complex may occur.(ABSTRACT TRUNCATED AT 250 WORDS)
Fifteen patients aged 10 to 18 years with syncope of unknown origin, and 10 healthy control children aged 11 to 18 years, were evaluated by head-up tilt to 60 degrees for 60 minutes. Six patients (43%) reproduced symptoms of syncope during the examination. Four had a typical vasovagal reaction; two had marked hyperventilation. None of the children in the control group had syncope. The head-up tilt test offers a simple, noninvasive, high-yielding diagnostic tool for evaluation of syncope in children.
The course of 357 balloon inflations performed during 38 angioplasties for single-vessel coronary artery disease was prospectively studied using continuous ECG recording. Ischemic ECG changes appeared during 91 percent of the inflations at a mean of 20 +/- 8 seconds after inflation and resolved in 97 percent of those at a mean of 11 +/- 5 seconds after deflation. Elevation of the plasma CPK level was found in six patients who had ischemic ECG changes for at least 7.8 minutes. The duration of ischemia did not exceed 5.4 minutes in any of the patients without CPK elevation. Resolution of the ischemic changes was delayed in patients with CPK elevation and in last vs initial inflations. We conclude that in patients with noninfarcted myocardium, ECG changes follow coronary occlusion and reflow very rapidly, detecting these coronary events with a high sensitivity. Lack of rapid regression predicts lack of reperfusion, and persistence of ischemia for more than 7.8 minutes is sufficient to cause myocardial necrosis.
A 63-year-old man had symptomatic deglutition-induced atrioventricular (A-V) block. There was also a coexistent mixed type carotid sinus hypersensitivity presenting as A-V block. No A-V nodal dysfunction was revealed during electrophysiologic studies. The vasodepressor response to carotid massage implies a central vagal hyperresponsiveness, which can also explain the cardioinhibitory responses to swallowing and carotid sinus massage, both possibly unmasked by posterior myocardial infarction.
Amiodarone in a low dose (200 mg/day) was administered alone or in combination with other type I antiarrhythmic drugs as a first-line agent in 33 patients with ventricular tachycardia (VT) (n = 24) or ventricular fibrillation (VF) (n = 9) secondary to coronary artery disease with healed myocardial infarction. There were 30 men and 3 women (mean age 69 +/- 9 years). Left ventricular ejection fraction ranged from 16 to 45% (mean 29 +/- 8). Therapy was guided by the results of electrophysiologic studies without the use of a control study (without drugs). Predischarge electrophysiologic studies revealed inducible sustained VT in 8 patients (24%), nonsustained VT in 7 and noninducible VT in 18 patients. Mean follow-up time was 27 +/- 7 months. Eleven patients (33%) died, 5 suddenly (15%) and 6 from nonarrhythmic causes. Five patients (15%) had nonfatal recurrences of VT. Life-table analysis showed that arrhythmic recurrences or fatalities (VT or sudden death) were related to the results of the predischarge electrophysiologic studies and not to the baseline arrhythmia (VT or VF). Toxicity from amiodarone was uncommon and no patient discontinued taking the drug.
Signal-averaged electrocardiograms were obtained in 53 consecutive patients with a first acute myocardial infarction (AMI) who survived the first 10 days of hospitalization. The recording was performed twice, at Day 1 and at Day 10 of hospitalization, in patients without bundle-branch block and who did not receive antiarrhythmic therapy. Signal-averaged ECGs were obtained with an instrument which analyzes the presence of late potentials (LP) in each individual precordial lead. There were 41 men and 12 women, mean age of 67 years. On Day 1, three patients had LP (5.6%). On Day 10, LP was recorded in 11 patients (21%). In only one patient was LP transient. Patients who developed LP by Day 10 (absent in Day 1) had statistically significant lower root mean square (rms) voltage and higher QRS duration than patients who did not develop LP on Day 10. In conclusion, in patients with a first AMI who survive the initial hospitalization period and are not in need of antiarrhythmic therapy have an incidence of LP of 21%. A predischarge recording is preferable since this will maximize the chances of detecting LP.
The purpose of this study was to determine the coronary angiographic correlations (specifically disease of the left anterior descending coronary artery) of reciprocal ST segment depression appearing during inferior acute myocardial infarction. Forty six patients (41 men and five women; mean age 56 years) were allocated into two groups based on the extent of precordial ST segment depression: widespread (V1-V6) ST depression v localised (V1-V4) ST depression. Patients with no reciprocal ST depression or patients with ST depression in V1-V4 but with ST elevation in V5 and V6 (inferolateral acute myocardial infarction) were excluded. All patients were catheterised during hospital admission for infarction. Twenty four of the 28 patients with ST depression in V1-V6 had significant lesions in the left anterior descending coronary artery whereas 16 of the 18 patients with ST depression in V1-V4 had insignificant or no lesions in the left anterior descending artery. The sensitivity, specificity, and positive and negative predictive values of widespread ST depression in predicting disease in the left anterior descending coronary artery were 92%, 80%, and 86% and 89% respectively. In patients with inferior acute myocardial infarction and precordial ST depression, the extent of ST depression is of clinical significance. Widespread (V1-V6) ST depression suggests disease of the left anterior descending coronary artery, whereas localised ST depression (V1-V4) indicates its absence.
To determine the impact of RV infarction on the prevalence and complexity of ventricular arrhythmias during inferior AMI, 57 patients with no prior MI were studied by 24-hour Holter monitoring on the first and tenth days of AMI. Based on radionuclear studies, patients were allocated into two groups: (1) group A, 21 patients (37 percent) with normal RVEF (greater than or equal to 40 percent); and (2) group B, 36 patients (63 percent) with depressed RVEF (less than 40 percent). There were no significant differences between the groups regarding age and LVEF. Values of RVEF were 47 +/- 6 percent and 31 +/- 6 percent, respectively (p less than 0.05). The RVEF had no influence on the prevalence and complexity of early and late arrhythmias. Stratification of patients in group B into two subgroups based on the extent of RV dysfunction did not reveal any differences in the occurrence of all forms of ectopy (when both groups were matched to group A). Therefore, patients with inferior AMI, with or without RV infarction, have a similar prevalence of arrhythmias. Ventricular ectopic beats may be related to the severity and spread of LV involvement, rather than to RV dysfunction.
Flecainide acetate was administered at a dose of 100 mg twice daily to 15 patients with drug-resistant ventricular ectopy. Eleven patients had evidence of organic heart disease. Left ventricular function was normal in 13 patients, and 2 patients had mild and moderate left ventricular dysfunction respectively. All patients underwent a control (off drugs) and a flecainide Holter ECG. Flecainide suppressed ventricular ectopy by greater than 70% in 13 patients (86.6%), suppressed bigeminal beats by greater than 90% in 13 (86.6%), suppressed ventricular couplets by greater than 90% in 12 of 14 patients (85.7%), and completely suppressed runs of nonsustained ventricular tachycardia in 6 of 9 patients (66.6%). In only one patient who showed a 69% suppression of ventricular ectopy did ventricular couplets increase. No side effects of the drug were noted. We conclude that flecainide at a dose of 100 mg twice daily is highly effective in suppressing ventricular ectopy that is resistant to other anti-arrhythmic agents.
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