Seismocardiography is not a new term.
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Biomedical subjects
Publications and source records attributed to S Zoneraich.
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Clinical, radiologic and histo-pathological observations have suggested that conduction disturbances (CD) are frequent in patients with calcified mitral annulus (CMA). To determine the incidence of CD, 65 consecutive patients with CMA were studied. Sixty-five normal individuals, matched for age and sex served as a control group. CMA has been identified by M-mode echocardiography, cross-sectional echo and image amplifier fluoroscopy. CD were present in 23 patients with CMA as compared to seven patients in the control group (p less than 0.01). Three patients developed complete atrioventricular block (4.6%) during hospitalization requiring artificial pacemakers. We conclude that, 1) early detection of CMA in the elderly is useful in predicting a higher incidence of CD. 2) Complete heart block is more frequent in patients with CMA. 3) Frequent ECG follow-up in these patients has proven to be useful in avoiding serious clinical complications.
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The atrial depolarization pattern was studied in 22 patients with Wolff-Parkinson-White and Lown-Ganong-Levine syndrome. The influence of the accessory pathways on the shape, magnitude and conduction pattern of the PSE loop was analyzed. An accurate evaluation of the beginning of the delta wave and of the P loop distortions was obtained by using high magnification (1 mV = 30 cm) recordings. The Frank lead system was used. The influence of atrial size (documented by echocardiography) on the PSE loop is emphasized. Special attention has been focused on the terminal vectors as compared to a control group. In Wolff-Parkinson-White syndrome the size of the PSE loop was smaller than in Lown-Ganong-Levine syndrome or in the normal group. When atrial conduction disturbances and/or atrial enlargement was present the PSE loop was larger and distorted. The terminal vectors were abnormally oriented in 75 percent of the patients with Wolff-Parkinson-White syndrome, but only in one with Lown-Ganong-Levine syndrome. The beginning of the delta wave in patients with Wolff-Parkinson-White syndrome was located to the left of the E point in all but two. When the "concertina" effect was present, the direction of the terminal vectors remained unchanged. In four patients with the Lown-Ganong-Levine syndrome, the PSE loop closed, and in three patients, a small opening was present. We suggest that the changes in contour, duration and amplitude of the PSE loop are due to an abnormal pattern of atrial depolorization in Wolff-Parkinson-White syndrome.
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The duration, contour, and amplitude of atrial flutter wave (f) was studied by electrocardiogram (ECG) and vectorcardiogram (VCG) in 32 patients and was related to the size of the left atrium (LA) measured by the echocardiogram (E). The following ECG parameters were analyzed: (1) the duration of left atrial depolarization, i.e., LA wave; (2) the amplitude of LA wave; (3) the surface area of LA wave; (4) maximum amplitude (A) of f in Leads 2 and V1. There was good correlation between LA size and the duration of depolarization and surface area (p less than 0.01), but the maximum amplitude of the f wave in Leads 2 and V1 failed to predict LA size. The post-conversion sinus P wave showed abnormal LA depolarization time (P greater than 0.12 sec.) in 62 per cent of patients with enlarged left atrium (ELA) and in 43 per cent of patients with normal size LA (NLA). The VCG of the flutter wave revealed two patterns, (1) an eliptical smooth fsE loop in 63 per cent of patients with NLA, and (2) distorted fsE loop in 67 per cent of patients with ELA. Both VCG patterns were subdivided in two subgroups according to the number and location of conduction delays. The VCG of post-conversion P wave confirmed conduction delays in both groups. We conclude that both the size of the left atrium and conduction delays play a basic role in the duration and contour of left atrial wave.
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Twenty-one patients with transvenous endocardial right ventricular pacemakers and one patient with epicardial right ventricular pacemaker inducing artificial left bundle branch block (LBBB) were studied with echocardiographic and vectorcardiographic techniques. Sixteen patients were found to have an initial very active posterior motion of the interventricular septum occurring within 70 msec. (range, 40 to 100 msec.) of the pacemaker artefact followed by posterior movement during the ejection period (Pattern A). Eighteen of 20 patients with clinical LBBB serving as a control group showed a dynamic posterior motion occurring within 40 msec. of the onset of QRS and preceding anterior (paradoxical) motion of the septum during ejection. In four patients, following the initial brief posterior septal movement, there was flat or anterior movement of the septum during the ejection period (Patern B). Two patients had myocardial infarction and one had atrial septal defect and epicardial right ventricular pacemaker. Only in two patients the initial brief posterior septal motion was not recorded before moving posteriorly during the ejection period (Pattern C). The different patterns of septal motion found in patients with artificial LBBB and in those with natural LBBB could be explained by differences in activation of the heart, as shown by vectorcardiography. Echocardiographic septal evaluation of patients with artificial pacemakers could have diagnostic implications in suggesting possible underlying complicating cardiac abnormalities.
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The volume overload type of heart often observed in endurance athletes, was simulate a diseased heart. We used a battery of noninvasive graphic techniques, i.e., echocardiogram, apexcardiogram, carotid pulse, electrocardiogram, vectorcardiogram, phonocardiogram, systolic time intervals, and treadmill stress testing in 12 professional marathon runners, mean age 33.8 +/- 11.1. Twenty nonathletes matched for age, height, sex, and weight served as a control group. Left ventricular (LV) end-diastolic dimension in marathon runners averaged 5.53 +/- 0.5 cm compared to 4.81 +/- 0.04 cm in nonathletes (p less than 0.001), LV end-diastolic volume was 172.69 +/- 43.3 ml compared to 113.57 +/- 30.41 ml in nonathletes (p less than 0.001), stroke volume was 122.27 +/- 32.8 ml compared to 78.42 +/- 20.44 ml in non-athletes (p less than 0.001), the thickness of the posterior LV wall was 1.0 +/- 0.2 cm compared to 0.7 +/- 0.1 cm in nonathletes (p less than 0.001), and LV mass was significantly increased, 212.43 +/- 55.8 g compared to 123.48 +/- 24.54 g in non-athletes (p less than 0.01). Left atrium and aortic root were also relatively larger in athletes (p less than 0.01). Right ventricular end-diastolic dimension was enlarged in marathon runners (2.02 +/- 0.65 cm). No statistically significant differences were noted in ejection fraction, percentage of internal diameter shortening (% delta D) and PEP/LVET. The carotid tracing had a bisferiens pulse in five marathon runners. The apexcardiogram showed a bifid systolic thrust in three and absence of abnormal A wave. These abnormalities were related to the overload type of heart as proven by echocardiogram. "Early repolarization syndrome" (abnormal RS-T segment elevation) and notched T waves in ECG had a counterpart a semilunar configuration in the VCG. Three athletes met ECG criteria and one met VCG criteria of LVH. The treadmill exercise ECG was negative in all 12 athletes. Biventricular enlargement and increased left ventricular mass are present in the marathon runner's heart. Myocardial contractility at rest was, however, not statistically different from nonathletes.
The diagnosis of ruptured aortic cusp leading to acute aortic insufficiency was made by echophonocardiographic techniques in a patient with nonvegetative aortic valvular endocarditis and a negative clinical history. Early closure of the mitral valve, weak first heart sound, tall A wave of apexcardiogram, and early diastolic murmur indicated acute aortic regurgitation. Fine high frequency echoes of the aortic root and aortic leaflets suggested ruptured aortic leafet unlike that reported in the presence of vegetations. Timing of S1 in acute aortic regurgitation by phonocardiogram, echocardiogram, and pulse techniques could not establish a single causative valvular relation in the genesis of this sound.
To examine left ventricular performance in diabetic patients without clinical evidence of cardiac involvement, systolic time intervals (pre-ejection period, left ventricular ejection time index and ratio of pre-ejection period to left ventricular ejection time) and echocardiographic measures (percentage changes in minor axis diameter, end-diastolic and end-systolic diameter, end- diastolic volume and end-systolic volumes, stroke volume and ejection fraction), were obtained. There were 89 diabetic patients and 93 control subjects evaluated for systolic time intervals, and 40 diabetic patients and 20 control subjects evaluated by echocardiogram. The diabetic group demonstrated significant (P less than 0.001) differences from the normal control group in each of the noninvasive measures of systolic time intervals. Pre-ejection period/left ventricular ejection time ration was increased by 25 percent and the pre-ejection period was increased by 12 percent in the diabetic patients. Among 40 diabetic patients studied by echocardiography, abnormal percentage change in minor axis diameter, (less than 30 percent) occurred in six individuals. Ejection fraction was decreased by 20 percent as compared to the control group, whereas end-diastolic pressure was not significantly different in the groups.
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New, poorly recognized echocardiographic findings were recorded in six patients with pericardial effusion. These findings were apparent prolapse of mitral and tricuspid valves, apparent systolic anterior motion of mitral valve, and midsystolic notching of pulmonic valve. Beat-to-beat variation of the dimensions of right and left ventricle and in the diastolic opening amplitude of the anterior mitral valve were present in cardiac tamponade. Substantial decrease or resolution of effusion resulted in disappearance of the observed abnormalities. Serial echographic studies before and after fluid resolution may prevent misleading echographic and clinical diagnoses.