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An electrocardiogram computer system significantly disagreed with itself in 36 of 92 pairs of unselected electrocardiograms which had not changed when recorded 1 minute apart.

Leads V1, V2 and sometimes V3 are omnibus leads that are "overburdened" because they monitor the left ventricular anterior wall, the left ventricular posterior wall, and the right ventricle; because they are the only leads normally expressing the ventricular gradient (QRS-T discordance); and because they consequently reflect numerous anatomic and electrical abnormalities and apparently normal variants. These require familiarity with and differentiation among a variety of pathologic and normal conditions.

Objectives: This study sought to find an association between dilated cardiomyopathy and limb-girdle muscular dystrophy., Background: Cardiomyopathy has been seen in various neuromuscular disorders, but it has not been recognized to be associated with limb-girdle muscular dystrophy., Methods: We investigated three sisters with well documented limb-girdle dystrophy and congestive heart failure by the 3rd decade of life. All underwent noninvasive evaluation of left ventricular systolic function by both echocardiography and radionuclide scanning, and one also had cardiac catheterization. Deoxyribonucleic acid (DNA) linkage analysis was performed in these affected subjects and in the unaffected family members, and DNA was extracted from mononuclear cells with primer sequences for three chromosome 13q microsatellite markers., Results: The parents had no evidence of clinical disease, but all three sisters had echocardiographic evidence of dilated cardiomyopathy. The sister with additional evidence of left ventricular dysfunction of cardiac catheterization had no coronary artery disease. The affected subjects had the same paternal allele for three potential markers of limb-girdle muscular dystrophy but different maternal alleles. The very small family size did not permit statistical confirmation or refutation of linkage for chromosome 13q markers., Conclusions: Demonstrable cardiomyopathy accompanying limb-girdle muscular dystrophy and its probable genetic associations require continued investigation by anticipating the cardiomyopathy in limb-girdle muscular dystrophy.

Objective: To systematically analyze the changes in mixed venous oxygen saturation (delta SvO2) during aortic operations with tube, aortobi-iliac, and aortobifemoral grafts., Design: Survey of consecutive patients., Setting: Teaching community hospital., Patients: Thirty-one patients (22 male, 9 female, mean age 67 +/- 10 yrs), undergoing elective operations for aortic aneurysms (n = 25) and aortoiliac occlusive disease (n = 6)., Interventions: SvO2 was recorded throughout the operation. Cardiac output, mean pulmonary arterial pressure, arterial oxygen saturation (SaO2), and arterial pH were measured before and immediately after the unclamping of the aortic graft., Results: In all patients, unclamping the aorta resulted in a marked reduction of mean SvO2, with no change in the cardiac output or SaO2. The unclamping of tube grafts was associated with a significant reduction in arterial pH (p less than .01) and in SvO2 (p less than .001), when compared with unclamping of bifurcation grafts. A significant (p less than .05) increase in mean pulmonary arterial pressure was observed after unclamping the aorta in patients with tube grafts. Despite a longer clamp time, unclamping the second limb of a bifurcation graft resulted in a smaller delta SvO2, when compared with that observed after unclamping the first limb (12% vs. 6%; p less than .01). The delta SvO2 after unclamping limb II was only 2% in aortobifemoral grafts and 9% in aortobi-iliac grafts., Conclusions: Reperfusion via extensive pelvic and lumbar collaterals in patients with aortoiliac occlusive disease reduces the delta SvO2 after aortic unclamping. Monitoring the changes in SvO2 during different types of aortic reconstruction helps to define precisely the physiologic alterations that occur in the course of these operations.

To elucidate the relationship between heart rate (HR) and left ventricular ejection time (LVET) during early exercise, 30 patients with chest pain were studied at 1 (1') and 4 minutes (4'). Mean results for control leads to 1' exercise: HR 79 to 105 beats per minute, LVET 247 to 260 msec. Thus instead of shortening as predicted by the HR change at 1' of exercise, LVET rose significantly (p less than 0.001). Subsequently LVET fell as HR continued rising, and by 4' had fallen toward control level. This phenomenon is comparable to the paradoxical decline in LVET as HR decreases early post-exercise and is comparably explained by transiently disproportionate change in determinants of LVET, stroke volume, and ejection rate. Absence of difference in response of exercise-positive (ST depression greater than or equal to 1 mm) and exercise-negative patients, also supports this initial paradoxical lengthening in LVET as a physiologic response.

In 12 normal subjects, use of ear densitography permitted measurement of systolic time intervals (STI) during uninterrupted treadmill exercise to over 90 percent maximal heart rate on a modified Bruce protocol. Results for control (sitting leads to standing) leads to end-exercise at 18 minutes leads to 10 minutes' sitting recovery were--heart rate (HR): (77 leads to 861 leads to 171 leads to 98 beats per minute; preejection period (PEP): (106 leads to 111) leads to 49 leads to 110 msec; ejection time index (ETI) (351 leads to 330) leads to 380 leads to 366 msec; PEP/LVET (0.42 leads to 0.49) leads to 0.29 leads to 0.45. Heart rate increased steadily to 18 minutes. In contrast, the PEP/LVET decrease was almost complete by three minutes and both ETI and PEP responses were bimodal with respective plateaus between three and six minutes and three and nine minutes. All STI and HR curves showed rapid restitution during early recovery. The changes during treadmill exercise were numerically comparable to those during bicycle exercise at a common heart rate. The results indicate that it is technically feasible to measure systolic time intervals with precision during uninterrupted treadmill exercise; responses to treadmill exercise were in the direction expected and quantitatively comparable to bicycle exercise at comparable stress level. These obervations provide the technical and physiologic bases for applying this method in clinical treadmill exercise testing.

Echocardiographic examination in a patient with primary pulmonary hypertension demonstrated midsystolic closure of the aortic valve, which has often been described in hypertrophic cardiomyopathy with or without obstruction, in discrete subaortic stenosis, and in ruptured aneurysm of the right coronary sinus of Valsalva. A possible mechanism for this finding in primary pulmonary hypertension and differential diagnosis from other diseases are discussed.

Within limits, systolic time intervals are reliable reflectors of cardiac status and responses to physiologic and pharmacologic challenges, with various functional correlates. That heart rate (HR) is an important determinant of the duration of systole is well accepted, owing to its effect on left ventricular ejection time (LVET). An independent rate effect on preejection period (PEP) is disputed. Some studies in pooled normal subjects at rest showed some degree of HR-PEP covariance, leading to widespread rate correction in practical use. However, although right atrial pacing showed the expected HR-LVET relation, it consistently failed to show an HR-PEP relation. Systolic time intervals were examined from echocardiograms of a deliberately heterogeneous group comprising 50 consecutively appearing persons with sinus rhythm. There was no HR-PEP covariance (r = 0.23; p = not significant). However, our subjects were otherwise comparable to those of other investigators, in that all other relations in these subjects were as expected from studies in both pooled and paced subjects: HR with LVET (r = -0.74; p less than 0.001), PEP/LVET with ejection fraction (r = -0.85; p less than 0.001), and PEP/LVET with velocity of circumferential fiber shortening (r = -0.65, p less than 0.001). Thus, HR correction of PEP is inappropriate. All other relations are substantiated in routinely encountered, unselected subjects.

Six instances of sudden death were recorded by Holter monitoring, which showed ventricular fibrillation in five and a bradyarrhythmia in one. Complex ventricular ectopic activity preceded cardiac arrest in five patients, including the one with the bradyarrhythmic arrest. Two patients with chronic bifascicular block arrested as a result of ventricular fibrillation. Fifteen cases reports from the literature are reviewed. The composite profile includes advanced myocardial disease (present in all cases), complex ventricular ectopic activity, R-on-T initiation of the terminal rhythm except in patients with prolonged QT interval, and variations in cycle length preceeding the onset of ventricular tachycardia or fibrillation. The role of supraventricular mechanisms in sudden death is uncertain.

Exercise responses depend on work load and its pattern of delivery. Administering a very brief ("impulse") load aims to elicit significant responses through biologic sensitivity to rate - rather than degree - of change. Electrocardiograms, systolic time intervals (STI) and heart rate (HR) were recorded continuously in 10 normal subjects during and after brief (20-sec) bicycle exercise at 50, 100 and 150 W. The purpose of this protocol was to identify a low load impulse-type exercise challenge which would be optimal in terms of (a) reproduction of the time course of exercise changes produced by longer duration (steady-state) exercise, (b) rapid achievement of quantitative responses reaching some or all of the steady-state changes at comparable work load, and (c) absence of ST changes in normal subjects. The onset of exercise produced the greatest rates of change. Directional changes and time course of all measurements paralleled those of steady-state exercise and recovery at the same loads: HR, ejection time index (ETI) and corrected ejection time (ETc) increased sharply; preejection period (PEP) and PEP/LVET fell sharply. Ejection time (LVET), stable through most of exercise, "paradoxically" decreased for up to 15 sec of recovery despite decreasing heart rates. For all measurements, restitution to control levels was complete by one minute of recovery.

Fourteen patients with pericardial effusions without clinical signs of tamponade (pulsus paradoxus or other cardiac and circulatory abnormalities) showed inspiratory reductions in echocardiographic left ventricular internal diastolic diameter which correlated directly with the exaggerated respiratory changes in systolic time intervals (both pre-ejection period and left ventricular ejection time). Excessive pericardial fluid affects left ventricular function even in the absence of clinical manifestations.

We report a rare electrocardiographic finding occurring in previously undescribed circumstances in which a 61-year-old man undergoing exercise testing developed striking ST segment elevation on the ECG characterized by electrical alternans of the ST segments. The significance of electrical alternans is briefly discussed in the light of this event.

Following exercise testing, a 71-year-old man developed atrial tachycardia with a unusual form of conduction disturbance: 4:2 atrioventricular (A-V) block. This pattern of A-V block is explainable by two different mechanisms of concealed conduction: two different levels of block in the A-V nodal region and dual A-V nodal pathways with concealed retrograde conduction of P waves. These concepts can also explain a variety of other unusual conduction disturbances.

Among 738 consecutive patients with chest pain referred for exercise testing, only 17 men fulfilled strict criteria for this pilot study: (1) achievement of at least 90 percent of age-predicted maximal heart rate or electrocardiographic criteria for a positive test; (2) subsequent coronary angiography; (3) exclusion of prior heart disease; and (4) absence of medication. Measurements of systolic time intervals obtained with ear densitography during early exercise differentiated 10 patients with coronary artery disease (Group 1) from 17 men (7 patients plus 10 normal volunteers) with normal coronary arteries (Group 2). Despite nearly identical heart rate and blood pressure responses in both groups, men in Group 1 had a significantly greater reduction of preejection period (PEP) at 1 minute and 4 minutes as well as a greater decrease in PEP/LVET (left ventricular ejection time) ratio. Differences were most significant when expressed as percent change of PEP/LVET ratio from control value (p less than 0.001 at both 1 minute and 4 minutes). After 4 minutes, men in Group 1 had no further decrease in PEP/LVET ratio and in 8 of the 10 men PEP/LVET ratio then increased to peak exercise. By contrast, PEP/LVET ratio continued to decrease to peak exercise in men in Group 2. The early floor in PEP/LVET ratio in Group 1 represents limited functional reserve and the subsequent increase suggests functional deterioration. Thus, densitographic systolic time interval measurements during uninterrupted exercise in unmedicated subjects appear to improve the sensitivity and specificity of the conventional treadmill test.

Fifty-four patients with a previous myocardial infarction and drug-refractory symptomatic ventricular tachycardia (VT) were treated with amiodarone on a long-term basis (range 6 to 54 months, mean 26) irrespective of the results of programmed ventricular stimulation, which was performed after high-dose oral amiodarone loading for more than 4 weeks. VT was rendered noninducible in 6 of 54 patients (11%) taking oral amiodarone. During a mean follow-up of 32 months, these 6 patients remained free of VT or sudden cardiac death. Forty-eight patients (89%) continued to have VT inducible by programmed ventricular stimulation. However, they could be separated into 2 groups: VT-modified (20 patients) and VT-unchanged (28 patients). In the VT-modified group, the induced VT with amiodarone was slowed or rendered nonsustained, and only 3 of 20 (15%) patients during a mean follow-up of 23 months had well tolerated VT recurrences. In the VT-unchanged group, 16 of 28 patients (57%) had recurrences of VT or ventricular fibrillation during a mean follow-up of 24 months. Sudden cardiac death occurred in 6 of these 16 patients. Thus, programmed ventricular stimulation in patients with VT taking long-term amiodarone may have prognostic implications.

A distinct late systolic "dip" in ventricular wall motion is described in patients with mitral valve prolapse. Sixty patients were referred because of clinically suspected mitral valve prolapse. Thirty of these patients had M-mode echocardiograms showing mitral valve prolapse. An abnormal late systolic "dip" in posterior wall motion was present at chordal level in 9 of 30 patients with prolapse but none of 27 patients without prolapse. All of these nine patients had late systolic prolapse and greater mean velocity of circumferential fiber shortening than 21 patients with prolapse but without the "dip" at chordal level (1.6 +/- 0.3 vs 1.3 +/- 0.2, p less than 0.02). Two of these nine patients had several episodes of transient cerebral ischemic attacks. Direct mural compression by the posterior chordae is offered as a possible mechanism for this echographic wall motion finding.

The efficacy and safety of a new antitachycardia pacing technique, self-adapting decremental overdrive pacing, was assessed in patients with clinical ventricular tachyarrhythmias who underwent programmed ventricular stimulation and serial drug testing. The three phases of this study involved a learning/experience phase, followed by intrapatient comparison of decremental overdrive pacing with conventional antitachycardia pacing modalities of overdrive burst ventricular pacing, and diastolic scanning with single (S2) and double (S2S3) ventricular extrastimuli. The final phase involved an intrapatient comparison of automated decremental overdrive pacing with overdrive burst ventricular pacing in patients with ventricular tachycardia (VT) cycle lengths of 280 msec or greater. Decremental overdrive pacing was superior to overdrive burst pacing and diastolic scanning (S2S3 and S2) (83% vs 38%, 50%, 9%) in patients with VT cycle lengths of 280 msec or greater. Automated decremental overdrive pacing as applied in the final phase was the most efficacious modality, terminating 92% of VT episodes compared with 56% for overdrive burst pacing in the same patients.

Arterial pH, Pco2, and osmolality were determined serially during cardiac resuscitation in patients and in dogs, with and without administration of sodium bicarbonate. These studies demonstrate that (1) in the absence of preexisting acidosis, severe acidosis can be prevented by adequate ventilation alone; (2) sodium bicarbonate administration results in a significant rise in arterial Pco2, which parallels the rise in pH despite adequate ventilation; (3) during prolonged cardiac and resuscitation, there is a rise in arterial osmolality that is accentuated by sodium bicarbonate. These studies suggest that sodium bicarbonate should not be used during resuscitation (1) in the absence of effective hyperventilation or where carbon dioxide removal is inadequate despite adequate ventilation, (2) in repeated doses, without confirmation of substantial acidosis, or (3) when cardiac arrest has been of brief duration and preexisting acidosis is unlikely. These studies also point to the need for a reappraisal of other buffers that do not elevate the arterial Pco2.

Contractile performance of ischemic feline myocardium was evaluated under conditions of selective changes in perfusate in pH and pCO2. A substantial increase in myocardial performance was noted when the pCO2 was lowered at constant pH, and depression of performance was noted when the pCO2 was increased at constant pH. Perfusate acidosis at constant pCO2 resulted in depression of performance and decreased performance only after 20 min of exposure. Alkalosis did not increase performance and decreased performance transiently during mild ischemia. These studies suggest that performance of myocardium during ischemia is closely related to tissue pCO2 and is minimally related to the level of extracellular pH.

The effect of oral propranolol on left ventricular performance during early upright exercise was evaluated by ear densitography in patients with arteriographic coronary artery disease (CAD). Measurements of systolic time intervals differentiated 10 unmedicated patients with CAD (group 1) and 15 patients with CAD taking propranolol (group 3). The patients in group 3 had less shortening of preejection period at 1 minute and 4 minutes of exercise than group 1 patients (p less than 0.001 and p less than 0.005, respectively), with propranolol appearing to prevent the abnormal shortening of preejection period seen in the unmedicated group. Group 3 patients, in contrast to group 1 patients, showed reduction of heart rate and heart rate-blood pressure product both at rest and during exercise. Furthermore, PEP/LVET and percentage change in PEP/LVET from control responses were similar to those of subjects free of CAD (group 2). These results indicate that propranolol effects a favorable change in LV performance by postponing early exhaustion of cardiac reserve, despite significant CAD. There was relatively large overlap in percentage change in PEP/LVET from control between group 2 and group 3 in contrast to the clear separation among unmedicated patients. Thus, the excellent diagnostic accuracy of systolic time intervals recorded during exercise is greatly reduced by beta-adrenoceptor blockade.