The omnicardiogram: New approach to detection of heart disease in patients with a normal resting electrocardiogram

The omnicardiogram is a new technique in which various leads of the standard electrocardiogram are digitized and subjected to a nonlinear mathematical transformation so as to detect subtle degrees of abnormality not apparent in the original electrocardiogram. Its usefulness in the detection of heart disease was studied in 121 male patients with a normal resting 12 lead electrocardiogram who underwent selective coronary cineangiography for a chest pain syndrome. In normotensive patients with a normal resting electrocardiogram, an abnormal omnicardiogram was recorded in 81 percent of those with three vessel disease, 67 percent of those with two vessel disease and 41 percent of those with one vessel disease. Nineteen percent of patients with normal coronary arteries or nonobstructive coronary artery disease had false positive tracings. The omnicardiogram was abnormal in 81 percent of patients with hypertension whether or not coronary artery disease was present. A double Master exercise test was performed by 109 of the 121 patients. In normotensive patients results of the test were positive in 67 percent of those with three vessel disease, 31 percent of those with two vessel disease and 14 percent of those with one vessel disease. There was a 4 percent rate of false positive tracings. Thus in our study, the omnicardiogram appeared to be superior to the Master test and to provide a useful new approach to detection of coronary artery disease in male patients with a normal resting electrocardiogram.     

Paradoxical motion of the interventricular septum with right ventricular dilatation in the absence of shunting: report of two cases.

A history, heart murmur, electrocardiogram and chest X-ray film suggesting an atrial septal defect associated with an echocardiogram revealing paradoxical motion of the interventricular septum with a dilated right ventricle may be considered indicative of a secundum or primum defect in a young adult or child. Two patients who fulfill all these criteria and had the presumptive diagnosis of an atrial septal defect were found at cardiac catheterization to have no demonstrable left to right shunt or other significant abnormality. The results of standard T-M mode echocardiograms were verified with B scan ultrasonograms. These cases may represent an early stage in the development of a cardiomyopathy. There is no echocardiogram pathognomonic of an atrial septal defect, and patients whose history and echocardiogram suggest this defect should have further diagnostic evaluation including technetium scan or cardiac catheterization.     

Correlations of electrocardiography and echocardiography in determination of left ventricular wall thickness: Study of apparently normal subjects.

To examine the usefulness of the surface electrocardiogram in predicting left ventricular wall thickness as determined with echocardiography, standard echocardiograms, electrocardiograms and Frank lead vectorcardiograms were obtained in 30 volunteers. End-diastolic thickness of the interventricular septum and free posterior wall was measured from the echocardiogram and compared with the sum of the S wave in lead V1 plus the R wave in lead V6 (VS1+R6) and the magnitude of the Frank lead vector (Vf), a scalar dunction obtained from a simple analog device. The maximum of Vf, the summated vector (Vf), was highly correlated with VS1+R6 (r=0.84). There was significant correlation between the summated vector and VS1+R6 and the thickness of the interventricular septum (IVS) (r=0.73 and 0.66, respectively). The best least mean square fit for the population was Vf=1.7 IVS-0.39. There was no significant correlation between these variables and the end-diastolic thickness of the posterior wall. Volunteers who were athletically inclined or were joggers tended to have larger summated vector values and evidence of symmetric or asymmetric left ventricular hypertrophy in the echocardiogram. It therefore appears that the thickness of the interventricular septum has a greater influence on the summated vector and VS1+R6 that the echocardiographically assessed thickness of the free posterior wall of the left ventricle. The implications of these findings in the light of recent reports about the incidence of echocardiographically diagnosed left ventricular hypertrophy are discussed.     

Value of Holter monitoring in assessing cardiac arrhythmias in symptomatic patients.

Holter electrocardiographic monitoring in 55 symptomatic patients with syncope, palpitations or dizziness uncovered significant arrhythmias in 30 patients (55 percent). By providing an observation period of at least 24 hours including a period of sleep, the procedure aided detection and diagnosis in both symptomatic and asymptomatic patients of transient arrhythmias or conduction abnormalities not documented by routine electrocardiograms. Bradyarrhythmias accounted for the majority of arrhythmias recorded in 21 or 30 symptomatic patients (70 percent); 15 had sinus bradycardia (35 to 55 beats/min) alone and 6 also had long episodes of sinus arrest of up to 5 seconds. Two had sinus bradycardia with periods of atrioventricular block with Wenckebach phenomenon. Five patients had a tachycardia-bradycardia syndrome; three had other episodic arrhythmias and one had pacemaker failure. In 15 (60 percent) of the 25 patients without arrhythmias, monitoring did not document the cause of symptoms. Holter monitoring is of considerable value in assessing the efficacy and adequacy of drug treatment, especially in patients with known heart disease, and in detecting pacemaker malfunction. However, very long periods of monitoring may be needed to make a diagnosis in those with only sporadic symptoms.     

Transient Q waves in Prinzmetal's angina

Transient abnormal Q waves were seen in two patients with Prinzmetal's angina during episodes of chest pain. The Q waves appeared recurrently while the patients had chest pain and disappeared when it subsided, indicating that Q waves suggestive of myocardial infarction can be seen with severe myocardial ischemia without actual necrosis. We describe these two patients, the various conditions in which transient abnormal Q waves have been reported and the theories offered to explain this electrophysiologic finding.     

Disappearance of abnormal Q waves after aortocoronary bypass surgery

Sixty-one patients were selected from 100 consecutive patients undergoing aortocoronary artery bypass. The number of vessels diseased as defined by coronary arteriography and the number of bypass grafts were recorded. Review of the preoperative electrocardiograms showed an infarct pattern in 26 of the 61 patients and analysis of the postoperative electrocardiograms revealed loss of abnormal Q waves in 3 of the 26. The pre- and postoperative clinical course of these three patients is analyzed and the extent of their coronary artery disease and number of bypass grafts compared with those of the 23 patients who had persistence of the infarction pattern and the 17 patients who manifested new Q waves. Possible explanations for the disappearance of abnormal Q waves are discussed.     

Bacterial endocarditis with ruptured sinus of valsalva and aorticocardiac fistula

A case is presented of bacterial endocarditis with a ruptured sinus of Valsalva and formation of an aorticocardiac fistula from the right coronary sinus into the right atrium and right ventricle. The pathologic, clinical and surgical aspects of bacterial endocarditis complicated by a ruptured sinus of Valsalva and an aorticocardiac fistula are analyzed. This complication of bacterial endocarditis is still uncommon, but alertness to its diagnosis makes possible early and successful surgical treatment.     

Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus erythematosus

Three patients, 24, 24 and 25 years of age, with systemic lupus erythematosus had signs of myocardial infarction. Two had serial electrocardiographic changes indicative of infarction without any cardiac symptoms. The third patient had clinical evidence of an acute massive myocardial infarction, which was proved at autopsy to be due to coronary atherosclerosis. This case is presented in detail and the association between systemic lupus erythematosus and myocardial infarction is reviewed. It is postulated that the relation between lupus erythematosus and coronary atherosclerosis is more than coincidental.     

Simulated left atrial tumor: A hemodynamic,echocardiographic and cineangiographic study

An experimental model of a prolapsing left atrial tumor mass has been utilized In dogs to study the hemodynamic events of the cardiac cycle and the cineangiographic and echocardiographic manifestations of this condition. The characteristic ventricular notch has been correlated with the timing of the expulsion of the simulated tumor mass from the left ventricle to the left atrium. The early notch seen with small simulated tumors delays aortic ejection by 0.02 to 0.03 second and results in abbreviated aortic ejection time and minimal distortion of the E-F slope of anterior mitral leaflet motion in the echocardiogram. Larger masses lead to late ventricular notching, transiently interrupt aortic flow and may displace the anterior mitral leaflet until It impinges on the interventricular septum in mid-diastole and at the onset of systole. A transient systolic Increment of coronary flow is observed after expulsion of the tumor from the left ventricle into the left atrium. There is an echo-free interval immediately after opening of the mitral valve, indicating that tumor motion lags perceptibly behind the initial blood flow through the mitral orifice. The sudden expulsion of the mass from the ventricle to the atrium early in systole represents an in vivo example of the quick release phenomenon.     

New Q waves after coronary artery bypass surgery for angina pectoris

Pre- and postoperative electrocardiograms were evaluated in 44 patients with angina pectoris who underwent single or multiple coronary artery bypass procedures. Two groups were identified: Group A, 37 patients with bypass procedures only, and Group B, 7 patients with bypass procedures and additional surgery (valve replacement in 4 and ventricular resection in 3).Preoperative electrocardiograms showed abnormal Q waves in 14 of 37 patients in Group A and in 3 of 7 patients in Group B. After coronary artery bypass, new Q waves appeared in 11 of 37 patients (30 percent) in Group A, including 1 of 9 (11 percent) with one-vessel disease on preoperative coronary arteriograms, 7 of 20 (35 percent) with, two-vessel disease and 3 of 8 (37.5 percent) with three-vessel disease; new intraventricular conduction abnormalities appeared in 4 of the 37. None of the seven patients in Group B had new Q waves postoperatively, but three had intraventricular conduction abnormalities. There was no correlation between new Q waves and preoperative values for left ventricular end-diastolic pressure. In Group A, new Q waves were demonstrated in 2 of 9 patients (22 percent) with one coronary bypass procedure, 5 of 21 patients (24 percent) with two bypass procedures and 4 of 6 patients (67 percent) with three bypass procedures. The single patient who had four coronary artery bypass procedures had no new Q waves after operation.It is evident that the prevalence of new Q waves was greater in patients who had two- or three-vessel disease by coronary arteriography as well as in those who had three coronary artery bypasses. Postoperative clinical course and mortality were not affected.     

Abnormalities of left ventricular function and geometry in adults with an atrial septal defect. Ventriculographic, hemodynamic and echocardiographic studies.

Left ventricular function and motion in 12 adults with an ostium secundum atrial septal defect were analyzed utilizing biplane cineangiography. Values for left ventricular end-diastolic volume index, stroke volume index, ejection fraction, left ventricular end-diastolic pressure and mean rate of circumferential fiber shortening were compared with values in an age-matched group of 11 normal subjects. Comparisons of ventriculographic and echocardiographic data were also made in 5 patients and 10 control subjects. Cardiac index was smaller in patients than in the normal subjects (3.6 vs. 4.5 liters/min per m2, P less than 0.01). Although left ventricular end-diastolic pressure was similar (8 mm Hg in both groups), the end-diastolic volume index was significantly smaller in patients than in normal subjects (56 vs. 76 ml/m2, P less than 0.05). Stroke volume index was also significantly smaller in patients (40 vs. 52 ml/m2, P less than 0.01). The two groups had similar values for ejection fraction (65 +/- 2 percent [standard error of the mean] in patients vs. 68 +/- 2 percent in normal subjects), circumferential fiber shortening velocity (1.67 +/- 0.13 vs. 1.81 +/- 0.15 circumferences/sec.), heart rate (91 +/- 7 vs. 90 +/- 5 beats/min) and mean systemic arterial pressure (92 +/- 5 vs. 87 +/- 3 mm Hg). Early systolic bulging of the upper ventricular septum toward the right ventricle was seen in 10 of 12 patients with an atrial septal defect but in no normal subject. Echocardiographic data supported these findings. No other abnormalities of motion were consistently noted. It is concluded that the left ventricle of patients with an atrial septal defect is subnormal in volume and abnormal in sequence of contraction of the septum and is characterized by apparent decreased distensibility.     

Calcium-membrane interactions in the myocardium: effects of ouabain, epinephrine and 3',5'-cyclic adenosine monophosphate

Cardiac microsomes, which represent an enriched but not pure preparation of the heart's sarcoplasmic reticulum, can remove calcium from solution by 2 kinetically dissimilar mechanisms. In the presence of adenosine triphosphate (ATP), Ca⁺⁺ is taken up by cardiac microsomes by a process designated Ca-binding, which exhibits saturation kinetics. The rate and extent of Ca-binding, and the high affinity of the Ca-binding sites could allow this process to cause the intact cell to relax. When anions that permit Ca⁺⁺ to be precipitated within the mlcrosomal vesicles are included along with ATP, much larger amounts of Ca⁺⁺ are taken up by cardiac microsomes. This second process, designated Ca-uptake, does not follow saturation kinetics. Instead, the rate of Ca-uptake increases linearly with increasing Ca⁺⁺ concentration until Ca-uptake becomes inhibited at higher Ca⁺⁺ concentrations.The finding of 2 kinetically distinct Ca⁺⁺ transport processes in cardiac microsomes, both of which are highly active in the micromolar range of Ca⁺⁺ concentration, suggests that Ca⁺⁺ movements in the intact myocardial cell may be controlled by 2 mechanisms. It is suggested that one of these, possibly manifest in vitro as Ca-binding, represents an intracellular release site that initiates systole by delivering Ca⁺⁺ to the contractile proteins. The second process, possibly manifest in vitro as Ca-uptake, is suggested to represent the uptake of Ca⁺⁺ into an intracellular storage site whose Ca⁺⁺ content indirectly determines the amount of Ca⁺⁺ that is delivered to the contractile proteins. These 2 intracellular Ca⁺⁺ pools can be tentatively related to Ca⁺⁺ movements into and out of the myocardial cell, permitting the formulation of a model by which a number of inotropic interventions might modulate myocardial contractility.Cardiac glycosides had no detectible effect on either cardiac microsomal Ca-binding or Ca-uptake. Cyclic adenosine monophosphate (cAMP), which by itself was without effects on cardiac microsomes, more than doubled the rate of Ca-uptake in the presence of a cyclic AMP-dependent protein kinase. The resulting increase in rate of Ca-uptake could explain the actions of epinephrine to enhance contractility at the same time that systole is abbreviated.     

Asymptomatic electrocardiographic alterations in sarcoidosis

Among 80 patients with tissue-confirmed sarcoidosis attending the sarcoidosis clinic of the Mount Sinai Hospital, electrocardiographic abnormalities of varying degree were noted in 41 patients, despite the fact that these patients were entirely without cardiac complaints and exhibited no evidence of previous or current cardiac disease on thorough examination. All these patients were under 40 years of age.The ECG alterations included repolarization abnormalities and alterations in rhythm and conduction. Because of the potential hazards of some of these abnormalities, prospective studies are being undertaken to determine which of them may represent precursors of dangerous intrinsic cardiac sarcoidosis.