Left ventricular aneurysm and congestive heart failure: Value of exercise stress and isosorbide dinitrate in predicting hemodynamic results of aneurysmectomy

In 12 patients with left ventricular aneurysm and chronic congestive heart failure, left ventricular functional reserve was assessed from the hemodynamic response to exercise stress after administration of isosorbide dinitrate. Two to 23 months (mean 8.6 months) after left ventricular aneurysmectomy hemodynamic measurements were made with the patient at rest and during exercise and were analyzed with respect to preoperative data. Left ventricular aneurysmectomy reduced mean left ventricular filling pressure from 25 to 17 mm Hg at rest (p < 0.02) and from 39 to 32 mm Hg during exercise (p < 0.05). There was no significant change in mean stroke volume index at rest or during exercise.Changes in resting and exercise hemodynamic indexes of left ventricular function produced by aneurysmectomy were inversely related to preoperative left ventricular function. Hence, hemodynamic status was less likely to improve In patients with good preoperative left ventricular function. Similarly, resting and exercise values for left ventricular function tended to improve in patients with reduced ejection fraction of the contractile section of the left ventricle. Left ventricular aneurysmectomy was generally effective in reducing left ventricular filling pressure but failed to achieve clinically important improvement in left ventricular performance during exercise. In patients with chronic congestive heart failure, left Ventricular aneurysmectomy should be performed only after careful assessment of preoperative left ventricular functional reserve.     

Implantable automatic scanning pacemaker for termination of supraventricular tachycardia

Thirteen patients suffering from reentrant supraventricular tachycardia have undergone implantation of a scanning extrastimulus pacemaker. This pacemaker is fully implanted and automatic, and it requires no external control device to activate or control it. The pacemaker is activated when tachycardia occurs. After four cycles an extrastimulus is induced with a preset coupling time from a sensed intracardiac potential, and every four cycles thereafter a further extrastimulus occurs, but on each occasion there is a decrement in coupling cycle by 6 ms until 90 ms of the cardiac cycle has been scanned by extrastimuli. When necessary, two extrastimuli can be introduced with a fixed but preset coupling time between them. Every four beats two extrastimuli are induced but the coupling time between the spontaneous cardiac potential and the first stimulus is decreased by 6 ms until 90 ms of the cardiac cycle has been scanned. The coupling time between the two stimuli is fixed throughout the scan. When termination of tachycardia occurs the successful timing variables are retained in the pacemaker memory so that at the onset of the next episode of tachycardia these settings are used first. Pacemaker pulse width, sensitivity, tachycardia trigger rate, coupling intervals for both stimuli and the use of single or double extrastimuli are all programmable transcutaneously.Three patients required single, and seven patients double ventricular premature stimuli; three patients required double atrial premature stimuli for termination of tachycardia. Despite frequent attacks of tachycardia before implantation, only two patients had a sustained attack of tachycardia after pacemaker implantation.     

Incessant atrioventricular tachycardia involving an accessory pathway: preoperative and intraoperative electrophysiologic studies and surgical correction.

In three patients with incessant supraventricular tachycardia, the anatomic substrate was a left-sided atrioventricular (A-V) accessory pathway. In two patients there was no expression of anterograde conduction through this pathway during spontaneous or induced atrial rhythms. The three patients had had increasingly frequent palpitations for more than 10 years despite adequate antiarrhythmic drug therapy.Preoperative intracardiac studies indicated that a left lateral accessory pathway was utilized in the retrograde limb of supraventricular tachycardia in all three patients. The spontaneous initiation of supraventricular tachycardia was due to (1) frequent spontaneous ventricular premature beats in two patients, (2) increase in sinus rate in two patients, and (3) ventriculoatrial reentry without preceding changes in sinus rate or intracardiac conduction intervals in one patient.At operation the accessory pathway was located in two patients with epicardial and endocardial electrographic mapping and cryothermal mapping. In one patient the His bundle was located with electrographic and cryothermal mapping. The accessory pathway (two patients) or the His bundle (one patient) were cryoablated by freezing over the area of the conducting tissue for 120 seconds at a temperature of ?65 ° C. Attempts to reinitiate supraventricular tachycardia after this procedure were unsuccessful. The operation was without significant morbidity. During follow-up for 3 to 10 months, no patient has experienced any further attacks of supraventricular tachycardia or required antiarrhythmic drugs.These observations confirm that an A-V accessory pathway may be the anatomic substrate for incessant or persistently repetitive tachycardias that may be resistant to medical and pacing therapy. Surgical interruption or cryothermal ablation of part of the reentrant circuit may abolish tachycardia, thus providing proof of the underlying mechanism.     

Cardiokymography during exercise testing: A new device for the detection of coronary artery disease and left ventricular wall motion abnormalities

The cardiokymograph (CKG) is a device that has been shown to reflect left ventricular (LV) wall motion abnormalities. Its accuracy in detecting coronary artery disease (CAD) during treadmill exercise testing was assessed in 204 consecutive patients undergoing coronary arteriography. Of the 188 patients with a technically adequate CKG, 146 (78%) had significant CAD. The sensitivity and specificity were similar for both the exercise electrocardiogram (ECG) (66% and 86%, respectively) and the exercise CKG (73% and 95%, respectively). An abnormal exercise CKG was significantly more common In patients with 3-vessel CAD than in those with 1-vessel disease (97% versus 52%, respectively;p < 0.001) and in patients with left anterior descending disease than in those without (85% versus 26%, respectively; p < 0.001). Seventy patients showed both an abnormal exercise ECG and CKG; all had CAD and 86% had multivessel CAD. Forty-eight patients demonstrated a normal exercise ECG and CKG; 29% had CAD but only 6% had multivessel CAD. Among 55 patients who had simultaneous exercise radionuclide ventriculography, new septal or apical wall motion abnormalities were found in 79% (23 of 29) of patients with an abnormal CKG compared with 19% (5 of 26) of patients with a normal CKG (p < 0.001). Thus, the CKG during exercise testing accurately reflects LV wall motion abnormalities and can be used to improve the diagnostic accuracy of exercise testing as an additional marker of myocardial ischemia.     

Proarrhythmic effects of the new antiarrhythmic agent flecainide acetate

Flecainide acetate, a new potent class I antiarrhythmic agent, was given to 152 patients (46 orally and 106 intravenously) over a period of 22 months. Seven patients developed proarrhythmic effects. The only conduction abnormalities induced were PR interval prolongation and QRS complex widening, and no patient developed significant sinus bradyarrhythmias; patients with known serious abnormalities of impulse generation or conduction were excluded from this study. Five patients developed ventricular tachycardia or ventricular fibrillation of whom only three had preexisting ventricular arrhythmias. QT and QT_c interval prolongation was observed but was due to QRS complex widening rather than to an increase in the JT interval. A patient with the Wolff-Parkinson-White syndrome had an inducible orthodromic atrioventricular (AV) tachycardia prior to flecainide, but only an antidromic tachycardia was induced after the drug. In one patient flecainide administration resulted in an increase of atrial flutter cycle length which resulted in development of 1:1 AV conduction and overall faster ventricular rate. Two patients who developed ventricular arrhythmias were taking other antiarrhythmic agents, and in this series proarrhythmic effects occurred with both normal and high flecainide concentrations.     

Relation of high-density lipoproteins to coronary artery disease

Low mean concentrations of high-density lipoprotein (HDL) cholesterol have long been recognized as a characteristic of patients with coronary heart disease, and the measurement of this fraction is a relatively strong discriminator between patients with coronary heart disease and those without. When subjects are ranked by the severity of coronary atherosclerosis determined angiographically, levels of HDL cholesterol, particularly of its HDL₂ subclass, are consistently lower in subjects with extensive disease than in those with minimal atheroma. HDL cholesterol is derived from a number of sources, mobilization from peripheral tissues being but one. Generally, longitudinal studies have confirmed that a low HDL cholesterol level is potently and independently predictive of a high risk of coronary heart disease, one exception being a study of subjects with hypercholesterolemia. Despite the strength of these epidemiologic associations, there is no evidence from experimental studies or clinical trials to establish that low HDL levels are causally important in atherogenesis.     

Is the treadmill exercise test useful for evaluating coronary artery disease in patients with complete left bundle branch block?

To aid in the study of coronary artery disease, 57 patients with complete left bundle branch block underwent clinical evaluation, treadmill exercise testing and cardiac catheterization. The patients were classified into two groups according to coronary anglographic findings: 30 patients with significant stenosis (70 percent or greater luminal narrowing) of at least one major vessel and 27 with no significant coronary artery disease. There was no difference in age, presenting symptoms or previous medical treatment between the two groups. There were more men in the group with coronary artery disease. Exercise-induced S-T changes were similar in the two groups; the sensitivity and specificity of these changes for the diagnosis of coronary artery disease were unacceptable irrespective of the criterion chosen. With additional S-T depression of either 1 or 2 mm below the baseline value, the predictive accuracy was only 53 percent. Combined exertional chest pain and 1 mm S-T depression increased the predictive accuracy of exercise testing to 71 percent. These data indicate that exercise-induced electrocardiographic changes do not facilitate detection of coronary artery disease in patients with complete left bundle branch block.     

Dopamine: its potential for inducing ischemic left ventricular dysfunction

As an agent potentially capable of inducing ischemia in patients with coronary artery disease, dopamine administered intravenously was evaluated as a pharmacologic stress agent by supine radionuclide angiography, and the results were compared with ergometer exercise. In a preliminary group of 11 subjects (4 normal subjects and 7 patients with coronary disease), dopamine alone was administered in increments of 2.5 micrograms/kg per min to a maximum of 15 micrograms/kg per min. There were significant differences between exercise and dopamine in maximal stress heart rates, 129.3 +/- 30.0 versus 88.0 +/- 35.8 beats/min (p less than 0.05) in normal subjects and 118.9 +/- 21.1 versus 87.6 +/- 22.6 beats/min (p less than 0.05) in patients with coronary disease, as well as in maximal stress rate-pressure products, 213.3 +/- 51.4 versus 155.0 +/- 52.5 mm Hg/min X 10(2) (p less than 0.02) in normal subjects and 216.0 +/- 45.6 versus 161.0 +/- 48.6 mm Hg/min X 10(2) (p less than 0.003) in patients with coronary disease. As a result, in these patients the ejection fraction response was significantly different: -3.3 +/- 4.5% with exercise versus + 6.3 +/- 4.6% with dopamine (p less than 0.05). In a second group of 41 subjects (9 normal subjects and 32 patients with coronary disease), atropine (0.6 mg) was administered intravenously before and after every second dopamine dose increment. This produced statistically similar maximal stress heart rates as compared with exercise in all subjects, rate-pressure products in normal subjects and slightly higher values with dopamine in patients with coronary disease: 200.3 +/- 47.2 versus 183.1 +/- 43.0 (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Pacing techniques in the management of supraventricular tachycardias. Part 2. An implanted atrial synchronous pacemaker with a short atrioventricular delay for the prevention of paroxysmal supraventricular tachycardias.

An implanted atrial synchronous pacemaker with an atrioventricular delay of 30 msec is described. This pacemaker was implanted into a patient with paroxysmal supraventricular tachycardia due to an intra AV nodal reciprocal mechanism. The pacemaker was able to trigger from atrial potentials following atrial premature beats down to a coupling time of 300 msec. Following each triggering atrial potential, a ventricular stimulus was applied 30 msec later thereby producing a ventricular premature beat in response to each sinus beat or each atrial premature beat. Retrograde conduction from this atrial premature beat blocked the re-entry mechanism within the AV node and prevented the initiation of tachycardia. A detailed discussion on all parameters of function of this pacemaker is presented.     

Septicemia in patients with an endocardial pacemaker.

The records of 1,235 consecutive patients treated with long-term pacing by the endocardial route between 1964 and 1977 were analyzed to determine the incidence, mechanism, course and treatment of septicemia. Septicemia developed in 12 patients (1 percent), and Staphylococcus aureus was isolated from the blood culture in 10. All patients were treated with the usual prolonged course of bactericidal drugs. Treatment was successful in only two of the seven patients whose endocardial pacing system was left in place; in three of the seven the septicemia recurred, necessitating removal of the endocardial system, and two of these patients died. In the remaining four patients the endocardial wire was promptly withdrawn, with use of a thoracotomy when necessary, and an epicardial system inserted; all of these patients survived. This is the treatment of choice.     

Glucagon secretion in unaffected monozygotic twins of juvenile diabetics.

Glucagon secretion during a 50-g oral glucose tolerance test has been investigated in 16 nondiabetic monozygotic twins of juvenile diabetics and compared with the results in 10 normal controls and 10 untreated, newly diagnosed, maturity-onset diabetics. Normal subjects showed a significant mean fall in glucagon at 15, 30, and 60 min, with a return to the baseline at 120 min. Maturity-onset diabetics showed a significant mean rise 15 min after oral glucose. The mean of the twin group was intermediate between normals and diabetics, although there was considerable individual variation with some showing suppression and others stimulation of glucagon release. When the twins were divided according to the length of discordance it was found that the mean response in the 8 twins who had been discordant for a mean of 19 years was indistinguishable from that of normal subjects, whereas the mean response of twins discordant for a mean of only 4.5 years was similar to that of the diabetic patients. It is possible, therefore, that hypersecretion of glucagon may occur in some subjects predisposed to develop diabetes mellitus, and the finding of lack of suppression of glucagon in the identical twin of a juvenile diabetic may be of prognostic significance. Identical twins who have been discordant for over 10 years are thought on other grounds to be unlikely to develop diabetes, and the finding of a normal glucagon response is further confirmation of their normal metabolic status and reinforces the suggestion that they are not prediabetic.     

Posterior wall velocity: an unreliable index of total left ventricular performance in patients with coronary artery disease

Posterior wall velocity determined by use of echocardiography has been proposed as an index of total left ventricular performance in patients with ischemic heart disease. Accordingly, in 9 normal subjects and 39 patients with angiographically documented coronary artery disease, we compared mean endocardial posterior wall velocity determined by echocardiography with echocardiographic and biplane cineangiographic calculations of ejection fraction and the mean rate of circumferential fiber shortening (mean V_CF), and with externally recorded systolic time intervals. All studies were performed on the same day in each patient. Mean endocardial posterior wall velocity averaged 4.6 cm/sec (range 2.9 to 8.7) and correlated poorly with echocardiographic ejection fraction (r = 0.47), cineanglographic ejection fraction (r = 0.26), cineangiographic mean V_CF (r = 0.47), the ratio of preejection period to left ventricular ejection time (r = ?0.35) and the preejection period corrected for heart rate (r = ?0.30). Substitution of maximal for mean endocardial posterior wall velocity did not improve the separation of normal from depressed left ventricular performance. Epicardial posterior wall velocity, a measurement more easily obtainable than endocardial posterior wall velocity, also did not correlate well with systolic time intervals or with ejection fraction or mean v_cf derived from the echocardiogram and cineangiogram. Both endocardial and epicardial posterior wall velocity values were poorly reproducible on a day to day or a beat to beat basis. We conclude that neither endocardial nor epicardial posterior wall velocity, whether derived as a mean or a maximum, provides an accurate measure of total left ventricular performance in patients with coronary artery disease.     

Determinants of arrhythmogenic ventricular activity detected on the body surface QRS in patients with coronary artery disease

The prevalence of arrhythmogenic ventricular activity (AVA) was investigated in 166 patients with coronary artery disease. Thirty patients had documented ventricular tachycardia (VT)/ventricular fibrillation (VF). Bipolar X, Y, Z leads were signal-averaged and filtered with a 40-Hz, bidirectional, high-pass digital filter. The filtered QRS signals were analyzed for the amplitude of the last 40 and 50 ms; duration of low-amplitude potentials (less than 40 microV) in the terminal portion; and duration of the filtered QRS. A positive AVA test result was defined as the presence of 2 or more abnormal indexes. Of the 30 patients with VT/VF, 66% had positive AVA test results (AVA-positive patients). Of the 136 patients without VT/VF, 25% had positive AVA test results. The following univariate variables showed significant correlation with an AVA-positive test: age, previous myocardial infarction, previous VT/VF, left ventricular wall motion abnormalities and left ventricular ejection fraction. Multivariate stepwise discriminant function analysis revealed that the presence of previous myocardial infarction and history of sustained VT/VF were the only independent determinants of AVA. During electrophysiologic studies, sustained VT/VF could be induced in 77% of the AVA-positive patients (24 of 31) and in 30% of the AVA-negative patients (3 of 10). The survival probabilities for 6, 12 and 18 months of follow-up were 92%, 85% and 85% for the AVA-positive and 97%, 92% and 90% for the AVA-negative patients. Our findings support the concept that a positive AVA test result reflects areas of delayed ventricular activation. The areas of delayed ventricular activation are associated with previous myocardial injury and scar tissue and serve as an anatomic basis for reentry.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relation of the echocardiographic estimate of left ventricular size to mortality in infants with severe left ventricular outflow obstruction

The relation of left ventricular size, as estimated with echocardiography, to mortality was evaluated in three groups of infants with severe left ventricular outflow obstruction. Group I consisted of 17 patients with combined aortic and mitral stenosis or atresia associated with definite hypoplasia of the left ventricle. Group II consisted of eight patients with the primary diagnosis of severe aortic stenosis. Group III consisted of 12 patients with severe coarctation of the aorta. The left ventricular enddiastolic dimension measured with M mode echocardiography and the cross-sectional area of the left ventricular cavity as seen in the parasternal long axis view of the two dimensional echocardiogram were used as indexes of left ventricular volume.All patients with symptomatic outflow obstruction and a left ventricular end-diastolic dimension of less than 13 mm died in infancy. However, five patients with a hypoplastic left ventricle proved at angiography or at autopsy, or both, were found to have a ventricular end-diastolic dimension of 13 mm or greater. Two dimensional echocardiography showed that the left ventricle in these patients was foreshortened and spherical in shape. The cross-sectional area of the left ventricle of each patient in group I was less than 1.6 cm². This was below the range of cross-sectional areas found in a group of normal infants (1.8 to 3.5 cm² ± 2 standard deviations about the mean). Three patients in groups II and III had a slightly reduced left ventricular area (1.7 cm²) and none of these patients survived infancy.Measurement of the cross-sectional area of the left ventricle is a useful method of determining left ventricular size in infants suspected of having the hypoplastic left ventricle syndrome. Patients who have reduced left ventricular volume as assessed by this technique are at very great risk even if surgical relief of the outflow obstruction is attempted.     

Effect of coronary artery bypass grafting on left ventricular response to isometric exercise

The left ventricular (LV) response to isometric exercise was evaluated in 20 patients who performed handgrip exercise tests before and 3 months after coronary artery bypass grafting. Preoperative LV ejection fraction (EF) decreased during the handgrip test from 0.57 +/- 0.08 to 0.49 +/- 0.09 (p less than 0.001); the ratio between the LV peak systolic pressure (PSP) and end-systolic volume index (ESVI) did not change. In 12 patients with patent grafts, the LVEF after operation did not change (0.54 +/- 0.06 at rest and 0.56 +/- 0.06 during handgrip exercise) and PSP/ESVI ratio increased from 4.5 +/- 1.5 to 5.6 +/- 2.1 mm Hg/ml X m-2 (p less than 0.001) during exercise. In 8 patients with occluded grafts, the LVEF after operation decreased from 0.56 +/- 0.10 to 0.48 +/- 0.06 (p less than 0.02), whereas PSP/ESVI did not change during handgrip exercise. Thus, the LV response to isometric handgrip exercise appears to improve after coronary artery bypass grafting in patients with patent grafts, but not in patients with 1 or more occluded grafts.