Edward G. Abinader

Quantification of atrial contribution to left ventricular filling by pulsed Doppler echocardiography and the effect of age in normal and diseased hearts

Atrial filling fraction, or the fraction of stroke volume resulting from atrial contraction, was measured by Doppler echocardiography from the time-velocity integral of mitral anulus inflow with a method that allows separation of conduit or passive flow from flow resulting from the atrial contraction. The method was validated in 17 patients with externally programmable ventricular demand pacemakers by showing that the time-velocity integral of passive flow (excluding the A wave) during sinus or sequential atrioventricular pacing was almost identical to the time-velocity integral during ventricular pacing. Atrial filling fractions were then measured in 41 normal subjects, aged 20 to 80 years; 28 patients with echocardiographic evidence of concentric left ventricular hypertrophy; 24 with dilated cardiomyopathy (13 of whom had an ischemic origin); and 19 with acute myocardial infarction. Atrial filling fraction increased significantly with age in normal subjects (r = 0.77; p less than 0.001) and ranged from 12% in a 20-year-old man to 46% in a normal 80-year-old woman. In the hypertrophy group, atrial filling fraction had a weak relation with age (r = 0.47; p = 0.006), and the values were significantly higher than in normal subjects. In patients with cardiomyopathy or infarction, atrial filling fraction varied over a wide range and showed no relation to age. Thus, atrial filling fraction as determined by Doppler echocardiography is significantly altered by both age and left ventricular disease. Age-corrected nomograms are essential when assessing atrial filling fraction in individual patients.

Nocturnal ischemic events in patients with obstructive sleep apnea syndrome and ischemic heart disease: effects of continuous positive air pressure treatment.

OBJECTIVES To investigate the occurrence of nocturnal ischemic events in patients with obstructive sleep apnea syndrome (OSAS) and ischemic heart disease (IHD). BACKGROUND Although previous reports documented nocturnal cardiac ischemic events among OSAS patients, the exact association between obstructive apneas and ischemia is not yet clear. It is also not known what differentiates between patients showing nocturnal ischemia and those that do not. METHODS Fifty-one sleep apnea patients (age 61.3+/-8.3) with IHD participated in the study (after withdrawal of beta-adrenergic blocking agents and anti-anginotic treatment). All patients underwent whole-night polysomnography including ambulatory blood pressure recordings (30 min interval) and continuous Holter monitoring during sleep. A control group of 17 OSAS patients free from IHD were also similarly studied. Fifteen of the 51 patients were also recorded under continuous positive airway pressure (CPAP). RESULTS Nocturnal ST segment depression occurred in 10 patients (a total of 15 events, 182 min), of whom six also had morning ischemia (06-08 am). Five additional patients had only morning ischemia. No ischemic events occurred in the control group. Age, sleep efficiency, oxygen desaturation, IHD severity and nocturnal-double product (DP) values were the main variables that significantly differentiated between patients who had ischemic events during sleep and those who did not. Nocturnal ischemia predominantly occurred during the rebreathing phase of the obstructive apneas, and it is characterized by increased heart rate (HR) and DP values. Treatment with continuous positive airway pressure significantly ameliorated the nocturnal ST depression time from 78 min to 33 min (p<0.001) as well as the maximal DP values (14,137+/-2,827 vs. 12,083+/-2,933, p<0.001). CONCLUSIONS Exacerbation of ischemic events during sleep in OSAS may be explained by the combination of increased myocardial oxygen consumption as indicated by increased DP values and decreased oxygen supply due to oxygen desaturation with peak hemodynamic changes during the rebreathing phase of the obstructive apnea. Treatment with CPAP ameliorated the nocturnal ischemia.

Anticardiolipin antibodies and acute myocardial infarction in non-systemic lupus erythmatosus patients: A controlled prospective study

PURPOSE To examine the prevalence of anticardiolipin antibodies (ACLA) in relatively young patients with acute myocardial infarction (MI) and their role in subsequent coronary and thromboembolic events in the post-MI period. PATIENTS AND METHODS In 124 relatively young survivors (aged 65 or younger) of acute MI, ACLA were measured in a controlled prospective study on admission and 3 months later. Myocardial reinfarction and thromboembolic events during a mean follow-up period of 19 +/- 3 months were diagnosed by standard tests. RESULTS Seventeen (14%) of the 124 patients were ACLA positive (either IgM or IgG) upon admission compared with 2 out of 76 (3%) of the control group matched for age and coronary risk factors (P < 0.01). The levels of ACLA remained unchanged in all but 1 patient 3 months later. During the follow-up period the rate of thromboembolic events and myocardial reinfarction was significantly higher in the ACLA-positive patients as compared with the ACLA-negative group: 41% versus 4% (P < 0.0001) and 35% versus 10% (P < 0.05), respectively. Using logistic regression, high titer of ACLA was found to be the only independent risk factor for subsequent thromboembolic events or myocardial reinfarction after acute MI. CONCLUSIONS High prevalence of ACLA was found in relatively young survivors of acute MI. The presence of ACLA is a marker for increased risk of subsequent myocardial reinfarction and thromboembolic events after acute MI.

Cerebrovascular accident complicating acute myocardial infarction: Incidence, clinical significance, and short-long-term mortality rates

Abstract purpose: The purpose of this study was to report the incidence, the antecedents, and the clinical significance of clinically recognized cerebrovascular accidents or transient ischemic attacks (CVA-TIA) complicating acute myocardial infarction. patients and methods: During 1981 to 1983, a secondary prevention study with nifedipine (SPRINT) was conducted in 14 hospitals in Israel among 2,276 survivors of acute myocardial infarction. During the study, demographic, historical, and medical data were collected on special forms for all patients with diagnosed acute myocardial infarction in 13 of these 14 hospitals (the SPRINT registry, n=5,839). Mortality followup was completed for 99% of hospital survivors for a mean follow-up of 5.5 years (range: 4.5 to 7 years). results: The incidence of CVA-TIA was 0.9% (54 of 5,839). The latter rate increased significantly only with age, from 0.4% among patients up to 59 years old to 1.6% among those aged greater than or equal to 70 years. Multivariate analysis identified age, congestive heart failure, and history of stroke as predictors of CVA-TIA during the acute phase of myocardial infarction. Patients with CVA-TIA exhibited a complicated hospital course, with a 15-day mortality rate of 41%. Subsequent mortality rates in survivors at 1 and 5 years were 34% and 59%, respectively. Rates at the same time points in patients without CVA-TIA were 16%,11%, and 29% (p conclusion: In this large cohort of consecutive patients with myocardial infarction, CVATIA was a relatively infrequent complication of acute myocardial infarction. Factors independently favoring the occurrence of CVA-TIA were old age, previous CVA, and congestive heart failure. CVA-TIA occurring during acute myocardial infarction independently increased the risk of early death threefold as well as the risk of long-term mortality in early-phase survivors (2.5-fold).

Continuous electrocardiographic monitoring with Holter electrocardiocorder throughout all stages of gastroscopy.

Continuous electrocardiographic recording on magnetic tape with a Holter electrocardiocorder was performed during gastroscopy on 55 consecutive patients. ECG recording was begun before premedication and was terminated 1 hr after the withdrawal of the gastroscope. The ECG changes during the different stages of the procedure were separately analyzed: 38.18% of patients had E.C.G. changes—sinus tachycardia (20%), ST-T changes (23.6%), ventricular and atrial premature beats (20.0% and 7.27%, respectively), atrial premature beats with aberrant conduction (3.6%), and coronary sinus rhythm (1.8%). All changes disappeared spontaneously after the procedure. Although relatively safe, gastroscopy requires careful consideration of the risks, especially in severe cardiac patients.

Dilated Inferior Vena Cava: A Common Echocardiographic Finding in Highly Trained Elite Athletes☆☆☆

Typical structural features of the athletes heart as defined by echocardiography have been extensively described; however, information concerning extracardiac structures such as the inferior vena cava (IVC) is scarce. Fifty-eight top-level athletes and 30 healthy members of a matched control group underwent a complete Doppler echocardiographic study. IVC diameter was determined in the subxiphoid approach 10 to 20 mm away from its junction to the right atrium. Measures reflect the median values between maximal inspiratory and expiratory values. IVC respiratory collapsibility index was determined as well. IVC in athletes was 2.31 +/- 0.46 cm compared with 1.14 +/- 0.13 cm in the control group (P <.001). Swimmers had an IVC diameter of 2.66 +/- 0.48 cm compared with 2.17 +/- 0.41 cm in other athletes (P <.05). The IVC was normal (/=2.6 cm) in 24.1% of athletes. The collapsibility index was 58% +/- 6.4% in athletes compared with 70.2% +/- 4.9% in the control group (P <. 001). Correlation was found between IVC size and VO(2) max (r = 0.81, P <.001) and the right ventricle (r = 0.81, P <.001) and with collapsibility index (r = -0.57, P <.05). Multiple regression analysis showed the impact of VO(2) max, cardiac index, and right ventricular and left ventricular end-diastolic dimensions on IVC diameter. IVC dilatation probably represents adaptation of an extracardiac structure to chronic strenuous exercise in top-level, elite athletes.

Atropine-induced ventricular fibrillation: Case report and review of the literature

A bradycardic and mildly hypotensive acute myocardial infarction patient developed sinus tachycardia, ventricular tachycardia, flutter, and fibrillation following intravenous atropine. Previous case reports are reviewed and the literature regarding the advisability of this mode of therapy is discussed. In the light of conflicting opinion as to the necessity of atropine in the mildly hypotensive and bradycardic acute myocardial infarction patient, and in view of its potentially deliterious effects on ischemic myocardium, a cautious and selective application of this drug is advised.

Adrenergic beta blockade and ECG changes in the systolic click murmur syndrome

In an attempt to elucidate the ECG changes associated with the SCMS, we have applied the propranolol test in 35 of our patients suffering from this syndrome. To the best of our knowledge this is the first such report in the English literature. Twenty-eight patients showed improvement and this points against an ischemic etiology. The test may be applied to differentiate ischemic ST-T changes from those associated with the SCMS. We have suggested the possibility of sympathetic overactivity and autonomic imbalance as the basis for the ECG and other features related to the SCMS. We have noted the striking similarities in the symptomatology and ECG changes associated with the SCMS and those of neurocirculatory asthenia. The implication of this was discussed.

Intrauterine diagnosis and control of fetal ventricular arrhythmia during labor

A very rare case of a sustained fetal ventricular arrythmia in the form of bigeminy, trigeminy, and quadrigeminy during labor is described. The rhythm distrubance failed to respond to sedatives and narcotics but was successfuly reverted to sinus rhythm following the administration of intravenous propranolol to the mother. The significance and possible mechanism of the arrhythmia is discussed.

Detection of diastolic atrioventricular valvular regurgitation by pulsed Doppler echocardiography and its association with complete heart block

Abstract The cineangiographic and hemodynamic presence of diastolic mitral regurgitation has been described in patients with complete heart block, aortic valvular regurgitation, hypertrophic cardiomyopathy, and in patients with long diastolic filling periods in atrial fibrillation. 1–3 However, because of its relatively low velocity, diastolic mitral regurgitation may be difficult to diagnose noninvasively. Pulsed Doppler echocardiography provides noninvasive evaluation of blood flow through cardiac valves and has been shown to be sensitive in the detection of valvular regurgitation. 4,5 We studied 8 consecutive, nonselected patients with complete heart block over a 6-month period, and all had Doppler evidence of diastolic mitral or tricuspid regurgitation.