Response of left atrial systolic function to handgrip in normal subjects.
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Biomedical subjects
Publications and source records attributed to J Gialafos.
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Doubts have been expressed about the clinical usefulness of time domain analysis of the signal averaged electrocardiogram in patients with prolonged QRS complex duration. We studied 147 patients using a signal averaged ECG (40-250 Hz) whose QRS complex was longer than 100 ms. A baseline electrophysiology study was also performed in 128 of these patients. Seventy-seven patients had a minor (QRS < 120 and > 100 ms) conduction defect. Thirty-seven of these 77 had either induced or spontaneous sustained ventricular tachycardia (group I) and 40 had no sustained ventricular tachycardia (group II). Seventy patients had a major (QRS > or = 120 ms) conduction defect, 44 of whom had sustained ventricular tachycardia (group A). The remaining 26 without this condition formed Group B. Group I compared to group II patients had a longer filtered QRS duration (120.8 +/- 14 vs 104.5 +/- 9.5 ms, P < 0.001), a longer low amplitude signal duration (41 +/- 12.1 vs 31 +/- 12.6 ms, P < 0.0001) and a lower root mean square of the last 40 ms of the filtered QRS complex (27 +/- 29.8 vs 35 +/- 25.3 microV, P = ns). Group A compared to group B had a longer filtered QRS duration (157.7 +/- 20.2 vs 140.7 +/- 15.7 ms, P < 0.001), a longer low amplitude signal duration (57.3 +/- 24.9 vs 37.8 +/- 20.3 ms P < 0.001) and a lower root mean square of the last 40 ms of the filtered QRS complex (14.3 +/- 11.2 vs 22.0 +/- 10.5 microV, P < 0.01). Using conventional late potential criteria, the sensitivity and specificity of the signal averaged ECG for the detection of sustained ventricular tachycardia patients with a minor conduction defect were 89% and 75%, respectively. The same criteria applied to patients with a major conduction defect were sensitive (sensitivity: 87%) but non-specific (specificity: 50%). However, by using modified late potential criteria, such as the presence of two of any of the following three signal averaged parameters: filtered QRS duration > or = 145 ms, low amplitude signal duration > or = 50 ms, root mean square of the last 40 ms of the filtered QRS complex < or = 17.5 microV, we derived a non-optimal but still acceptable combination of sensitivity (68%) and specificity (73%). We conclude that traditional late potential criteria can be applied in patients with a minor conduction defect, but modification of these criteria is necessary to derive useful clinical information for risk stratification of patients with a QRS complex duration > or = 120 ms.
We studied 12 patients (eight females and four males), ages 30-46 years, with echocardiographically documented mitral valve prolapse and clinical suspicion of coronary artery disease, based on a history of chest pain (five patients), angina-like pain (three patients), a positive exercise stress electrocardiogram (12 patients) and a focally positive thallium-201 stress perfusion scan (three patients), who were referred for cardiac catheterization and found to have normal coronary arteries. Ten patients without evidence of heart disease served as controls. In all mitral valve prolapse patients, coronary flow velocity reserve was determined successively in the left anterior descending, left circumflex and right coronary arteries as the ratio of the maximum (after intracoronary papaverine) to the resting mean coronary flow velocity. Coronary flow reserve values were fairly similar in the mitral valve prolapse and control patients; all 12 mitral valve prolapse patients had normal coronary flow reserve ( > or = 3.5) in all three coronary arteries with no significant differences among the arteries tested. Mean values +/- 1 standard deviation of the coronary flow reserve (mitral valve prolapse vs control patients) were 4.7 +/- 0.5 vs 4.6 +/- 0.6 for the left anterior descending, 4.6 +/- 0.4 vs 4.6 +/- 0.3 for the left circumflex and 4.5 +/- 0.4 vs 4.4 +/- 0.5 for the right coronary artery (all P = non-significant). The subsets of mitral valve prolapse patients with different clinical "ischaemic' manifestations were similar in terms of the calculated coronary flow reserve in all three major epicardial coronary arteries. In conclusion, this study demonstrated that an inadequate regional coronary flow reserve does not account for the clinical manifestations of myocardial ischaemia and positive exercise tests in patients with mitral valve prolapse and normal coronary arteries.
We present three cases of an unusual pacing lead aberration occurring at different times after implantation. In the first patient, the electrode was twisted close to the pacemaker, and dislodgment occurred on the 40th postoperative day. In the second case, there was only proximal twisting of the electrode. In the third case the electrode was twisted in two places: proximal to the pacemaker, and distal, within the right atrium. The complication was managed successfully by reimplanting the same electrode after stiffening the lead near the generator with a portion of the stylet.
We present a case of life-threatening arrhythmia occurring during tilt table testing in a 44-year-old man with syncope. Polymorphic ventricular tachycardia occurred while the patient was tilted up under the intravenous infusion of isoproterenol (2 micrograms/min). No ischemia, QTc prolongation, or electrolyte abnormality preceded this event. The arrhythmia was not induced by programmed ventricular stimulation or exercise testing. Based on electrophysiological and clinical data, the diagnosis of sick sinus syndrome was entertained.
The hematological profile of 12 patients with acute myocardial infarction and normal coronary arteriographic findings was compared to that of 8 patients with acute myocardial infarction associated with obstructive coronary artery disease, and of 12 patients with no evidence of myocardial infarction and normal coronary arteriographic and left ventriculographic findings who served as control. There were no significant differences in the hematological profile among the 3 groups, suggesting lack of a thrombotic tendency in patients with acute myocardial infarction and normal coronary arteriographic findings.
We studied the relation of left atrial mechanical function to the hormonal response in 14 patients with idiopathic dilated cardiomyopathy. Left atrial volumes were echocardiographically measured at mitral valve opening (maximal), at onset of atrial systole (onset of the P wave of the electrocardiogram) and at mitral valve closure (minimal) from the apical 2- and 4-chamber views using the biplane area-length method. Left atrial systolic function was assessed with the left atrial active emptying fraction ([volume at onset of atrial systole-minimal]/[volume at onset of atrial systole]). Plasma renin activity, aldosterone and atrial natriuretic peptide plasma levels were determined using commercially available kits. Left atrial maximal volume was directly, and left atrial active emptying fraction was inversely related to plasma renin activity (r = 0.60, P = 0.02 and r = -0.59, P = 0.026, respectively), aldosterone (r = 0.61, P = 0.02 and r = -0.53, P = 0.048) and atrial natriuretic factor (r = 0.79, P = 0.0009 and r = -0.62, P = 0.01) plasma levels. Thus, increased left atrial size and depressed left atrial contractile performance are associated with increased hormonal response in idiopathic dilated cardiomyopathy.
A case of what was assumed to be twiddler's syndrome was caused by spontaneous twisting and displacement of the electrode on the fortieth postoperative day. The pacemaker had not been manipulated by the patient, the pocket was tight, and the proximal electrode was well secured. The complication was managed successfully by reimplanting the same electrode after stiffening the lead near the generator with a portion of the stylet.
The standard exercise tests are usually inadequate for revealing the nature of oversensing problems associated with skeletal muscle myopotentials. We used special exercises, designed to test the rectus abdominis (RA) and pectoralis major (PM) muscle groups specifically, in a study of a large number of paced patients. We examined a total of 252 paced patients, with or without symptoms and in steady pacing rhythm, for the occurrence of pacemaker inhibition (215 VVI, 15 VVI Activitrax and 22 DDD, from 9 different manufacturers). Inhibition was observed in 75 (34.9%) of the conventional VVI, in 4 (26.6%) of the VVI Activitrax and in 17 (77.3%) of the DDD paced patients. It was found that both the PM and RA were capable of causing inhibition alone in some cases, while in others a synergy of the two groups was required. It is clear that the RA must always be considered as a possible serious source of inhibiting myopotentials, irrespective of the location of the pacemaker. The most effective exercise for eliciting PM exertion was pulling the flexed arm towards the chest against resistance, while in the supine position. For RA exertion, the best exercise was raising the head and trunk from the supine position and holding the trunk at an angle of about 30 degrees to the horizontal. Both these exercises gave good, consistently reproducible results.
The inhibition of unipolar demand pacemakers by myopotentials was studied in 215 paced patients with or without symptoms and in steady pacing rhythm. ECG recordings were taken of all patients at rest and during effort in which maximal muscular strength from the pectoralis major (PM) and rectus abdominis (RA) muscles was required. In 75 patients (34.9%) transient pacing inhibition was observed. In these patients myopotentials from the PM and RA muscles were recorded simultaneously at rest and during special effort. The PM was the dominant source of inhibiting myopotentials in 50.7% of the total patients with oversensing and the RA was dominant in 28%. In the remaining 21.3%, neither of these muscle groups alone was able to cause inhibition and a clear synergy of both the PM and RA muscles was required. When oversensing occurred in a pacemaker implanted in the thoracic wall, the PM was the dominant cause in 54.4% of patients and the RA in 23.5%, while a synergy of both muscles was required in the remaining 22%. When the pacemaker was implanted in the abdominal wall, the RA was the dominant source of inhibiting myopotentials in all but two patients.
We examined four patients with a demand pacemaker who exhibited transient symptoms of vertigo while trying to rise from the supine position. In two of these there was an epicardial pacing system with the pacemaker in the abdominal wall superficial to the rectus abdominis muscle; in the other two cases the pacing system was transvenous with the pacemaker superficial to the right pectoralis major muscle. It was found that the "pseudovertigo" was due to pacemaker inhibition caused by rectus abdominis myopotentials in all four patients. Changing the pacing mode from the demand to fixed-rate resulted in the disappearance of all symptoms at rest and during exercise.
Two cases with coupled ectopic ventricular rhythm associated with artificial pacing are presented. The premature ventricular beats appeared at a fixed distance from the R of the previous electrical stimulus complex and when pacing was stopped ventricular arrest occurred. This provides strong evidence that the ectopic ventricular beats were dependent on the electrical stimulus and therefore that they were produced by its re-entry. It was observed that the re-entry phenomenon occurred at low rates. This arrhythmia even persisted after the permanent pacing and was successfully suppressed by procainamide in both cases.
The right ventricular angiocardiographic findings, in the anterioposterior projection, are described on three patients with tricuspid valvular stenosis. During diastole, the tricuspid valve was delineated as an arcline contour, placed between the non opacified right atrium and the opacified right ventricle, and it was displaced to the left of the spine. Its mobility was diminished. Right ventricular angiocardiography seems to be a useful method for the diagnosis of the tricuspid valvular stenosis and the estimation of the pathology and the functional condition of the tricuspid valve. The method is recommended for further evaluation.
The left ventricular haemodynamic alterations during right atrial pacing were studied in 12 cases. Cardiac index varied little: during maximal rate however, its mean value was slightly lower than the resting one. Stroke index decreased inversely to the heart rate. The course of these indices did not separate the normal from abnormal cases. Ventricular function curves (VFCs) were constructed by relating the changes of left ventricular (LV) end-diastolic pressure (EDP) to those of stroke index (SI). In 4 normal cases the curves were steep, showing a fall of EDP with relatively large decrease of SI; in 3 cases of congestive myocardiopathy they were flat, showing fall of EDP in two and increase in one, with relatively small decrease of SI; in 5 patients with effort angina LVEDP initially decreased. This initial fall of VFCs was steep in two with normal and flattened in three with impaired resting LV function. Increase of EDP, evidently due to development of ischaemia, followed in all; it exceeded resting EDP in two out of three cases developing angina and in one out of two not developing angina. Our findings support the view that the increase of LVEDP is due to decrease of both myocardial contractility and compliance.
The effect of increasing heart rate by right atrial pacing on the peak value of the first derivative of left ventricular (LV) pressure(dp/dt) and the maximal velocity of the contractile element (KVmax) was studied in 12 cases. Peak dp/dt was poor as regards its sensitivity in reflecting the changes of contractility, due to its strong dependence on LV end-diastolic (EDP) and systolic pressure. KVmax increased constantly in the 4 normals and in 2 cases of ischaemic heart disease which did not develop angina; the increase exceeded 90 ml sec-1 in the former and one of the latter cases in which resting LV function was normal. In contrast, it decreased during the development of ischaemia in two of the three cases which developed angina; in the third case, in which also resting LV function was seriously impaired, the course of KVmax was almost flat. A similar flat course was observed in the three cases of congestive myocardiopathy. the above alterations of KV max were independent of the EDP and proportional to the basic contractility and its anticipated changes during pacing.
From 1972-1975, 232 consecutive patients suffering from A/V block were paced intravenously in the Cardiac Department. Medical School, University of Athens. Of these, 124 were female and 108 male. Their age range was between 49 and 85 years. Besides fluoroscopic and threshold control, the intraventricular electrocardiogram (E.C.G.)., recorded from the tip of the electrode, was used as a guide for the accurate positioning of the catheter-electrode in the right ventricle. An injury pattern with an elevation of the ST segment of at least 3 mV and characteristic and steady morphology was obtained when the electrode tip was satisfactorily impacted in the right position. As a consequence of this, an initial stimulation threshold below 0.7 mA was obtained in all cases and pacing failure, due to catheter displacement was noted in only 11 cases (5%), without any apparent increase in the incidence of right ventricular perforation.
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