Bradyarrhythmias: clinical significance and management

Clinicians have long recognized the potentially serious manifestations of extreme bradycardia. However, even marked bradycardia can often be physiologic, and in the presence of impaired ventricular function may offer important compensatory hemodynamic effects. Disorders of the sinoatrial node producing bradycardia include failure of impulse formation, sinoatrial conduction block, concealed sinus-perinodal reentry, carotid sinus hypersensitivity and the constellation of brady- and tachyarrhythmias that compose the "sick sinus syndrome." Bradycardia can also result from intraatrial block, atrioventricular nodal block or infranodal block. In addition, paroxysmal supraventricular tachyarrhythmias may produce concealment into the atrioventricular junction and simultaneous suppression of sinus node rhythmicity, resulting in long pauses. Pseudobradycardias manifesting as slow peripheral pulse rates can result from frequent, nonconducted early atrial premature beats, from ventricular bigeminy or runs of ventricular extrasystoles or from mechanical alternans. Cardiac pacemakers play an important role in the management of patients with severe symptoms attributable to bradyarrhythmias. However, excessive use of pacemakers and the inappropriate selection of physiologically unfavorable pacemaker systems should be avoided. Frequently, patients who are only mildly symptomatic with bradycardia should not receive a cardiac pacemaker because the prognosis is favorable. Patients with the tachy-bradycardia syndrome often require both pharmacologic and pacemaker therapy. In selected patients electrophysiologic testing may be helpful, but the majority of patients are best managed by careful attention to the history, electrocardiogram and ambulatory electrocardiographic recordings.     

Origin of so-called right and left ventricular arrhythmias in acute myocardial ischemia

The anatomic origin of ventricular arrhythmias occurring immediately after coronary arterial ligation was studied in 32 dogs. The electrocardiogram and seven single or composite bipolar electrograms were recorded from various sites within and surrounding the ischemic area in the left and right ventricles. Delay and fragmentation in the activation of the epicardial ischemic zone of the left ventricle, bridging diastole, preceded the appearance of ventricular arrhythmias and were continuous during the rhythm disorders. So-called left and right ventricular arrhythmias were associated with similar delay and fragmentation in left ventricular ischemic epicardial activity. Multiple and simultaneous activation of both the right and left ventricles produced ventricular fusion premature complexes. Multiple exit points increased before ventricular fibrillation occurred. The ultimate origin of premature ectopic impulse formation in the ventricles is not necessarily related to one or more exit points in either ventricle. Ischemic damage to the heart produces ventricular arrhythmias that appear to originate from both ventricles. The site of origin of ventricular arrhythmias should not be the sole factor in assessing the benign or malignant properties of the arrhythmia.     

Echocardiographic features of atrioventricular and ventriculoatrial conduction

The potential application of diagnostic ultrasound to understanding of the hemodynamic effects of various rhythm and conduction disturbances has not been fully explored. To investigate the changes in cardiac function associated with various atrioventricular (A-V) sequencing intervals during cardiac pacing, simultaneous M mode and two dimensional echocardiographic and hemodynamic studies were performed in 23 dogs.One to one A-V and ventriculoatrial (V-A) sequential pacing at cycle lengths of 400 and 300 ms revealed a stepwise reduction in left ventricular pressure and cardiac output as the A-V interval was changed from +100 to —100 ms. These reductions in cardiac hemodynamics were associated with decreases in left ventricular and increases in left atrial dimensions determined with echocardiography. Mitral valve excursion and the duration of valve opening remained constant over the entire range of A-V intervals. There was angiographie evidence of retrograde blood flow from the left atrium into the pulmonary venous system at an A-V interval of —50 and —100 ms, but no evidence of mitral regurgitation.Thus, correlative echocardiographic and hemodynamic studies can suggest multiple pathophysiologic mechanisms contributing to the decrements in cardiac function observed during tachyarrhythmias with intact A-V conduction as well as those occurring consequent to A-V nodal Wenckebach cycles.     

Polymorphous ventricular tachycardia associated with normal and long Q-T intervals

Polymorphous ventricular tachycardia may occur in the setting of either a normal or a prolonged Q-T interval. Torsade de pointes is a form of polymorphous ventricular tachycardia in which the polarity of the QRS complex exhibits phasic alterations in both axis and rate. Traditionally, torsade de pointes has been described in association with a variety of congenital and acquired (including drug and metabolic) causes of Q-T prolongation. The distinction between torsade de pointes and those polymorphous ventricular tachycardias occurring in patients with a normal Q-T interval has important therapeutic implications. The former requires strict avoidance of all drugs that may potentially further delay repolarization, including class I antiarrhythmic agents; immediately, the initiation of cardiac pacing is often necessary for control of arrhythmia, and on a long-term basis, sympathetic nervous blockade is often efficacious. In contrast, the polymorphous ventricular tachycardias with a normal Q-T interval usually respond to conventional therapy, including administration of class I antiarrhythmic agents. Thus, the management of polymorphous ventricular tachycardia should be based on the presence or absence of associated repolarization alterations rather than on the morphologic features of the tachycardia. Unfortunately, recent advances in basic and clinical electrophysiology have not yet elucidated the pathophysiologic basis for these arrhythmias, although this is an area of active investigative interest.     

Echocardiographic detection of coronary artery disease: Detection of effects of ischemia on regional myocardial wall motion and visualization of left main coronary artery disease

M mode and cross-sectional echocardiographic studies at rest have been used to detect regional left ventricular wall motion abnormalities as a sign of hemodynamically significant coronary artery disease. These techniques have proved to be fairly specific but not highly sensitive. Detection of new regional wall motion abnormalities with cross-sectional echocardiography during exercise appeared practical in 80 percent of patients in preliminary studies; the finding of such abnormalities is highly specific for the presence of coronary artery disease and, with this approach, the sensitivity of echocardiography is improved. Thus, patients with anatomically severe coronary artery disease on angiography may not manifest an echocardiographic abnormality in regional wall motion even during exercise. The direct noninvasive detection of the left main coronary artery in up to 90 percent of patients studied with cross-sectional echocardiography using the short axis or apical approach, or both, has been well defined. A high sensitivity and specificity of detecting anatomically severe left main coronary artery disease using the criteria of both luminal impingement and the presence of high intensity echoes have been confirmed. Further advances in imaging techniques may allow for better definition of the coronary arterial treë.     

Amelioration by nitroglycerin of left ventricular ischemia induced by percutaneous transluminal coronary angioplasty: assessment by hemodynamic variables and left ventriculography

Increasingly longer balloon inflation times during coronary angioplasty can create significant left ventricular ischemia, amelioration of which was attempted in this study using nitroglycerin. Hemodynamic variables were assessed during inflation of an angioplasty balloon in the proximal left anterior descending coronary artery of 10 patients. Regional wall motion was assessed by left ventriculography during a separate balloon inflation. Nitroglycerin (200 micrograms) was then administered intravenously, and hemodynamic and ventriculographic assessments during balloon inflations were repeated. Balloon inflation resulted in a marked increase in left ventricular end-diastolic pressure (from 9.2 +/- 2.1 to 19.4 +/- 2.9 mm Hg) and time constant of left ventricular relaxation (from 44.2 +/- 6.2 to 62.3 +/- 11.3 ms) and a decrease in distal coronary artery perfusion pressure (from 54 +/- 9 to 33.1 +/- 4 mm Hg). Time to onset of angina was 29 +/- 3 seconds and time to ST segment depression of 1 mm or greater was 30 +/- 3 seconds. Regional wall motion analysis 30 seconds after onset of balloon inflation revealed marked hypokinesia and akinesia in the anteroapical segments with graduated depression of inferior wall motion, greatest at the apex. After the administration of nitroglycerin, balloon inflation resulted in a smaller increase in end-diastolic pressure (from 5.0 +/- 2.7 to 8.3 +/- 2.6 mm Hg) and time constant (from 47.9 +/- 4.7 to 54.4 +/- 9.2 ms; both p less than 0.01 versus standard balloon inflation). Distal coronary artery pressure remained similar to standard balloon inflation (32 +/- 3 mm Hg) despite lower mean arterial pressure (89 +/- 5 mm Hg, p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Exercise cross-sectional echocardiographic diagnosis of coronary artery disease

To test the feasibility of detecting transient left ventricular regional wall motion abnormalities during exercise-induced myocardial ischemia, 55 patients undergoing diagnostic coronary arteriography were studied in a prospective blinded manner with wide angle cross-sectional echocardiography. The ultrasonic studies were obtained with the patients at rest and during exercise in the supine position using a bicycle ergometer. Cross-sectional echocardiographic studies during exercise were adequate for analysis in 43 (78 percent) of the 55 patients. Forty-one of the 43 manifested either a new regional wall motion abnormality during exercise (20 subjects) or wall motion that remained entirely normal during exercise (21 subjects); In two subjects an abnormal wall motion abnormality at rest did not change with exercise. Nineteen of the 20 patients with a new regional wall motion abnormality had significant coronary artery disease and 15 of these 19 had S-T segment depression during bicycle ergometry. The one patient with a normal coronary arteriogram had an early cardiomyopathy. Ten of the 21 subjects with normal wall motion at rest and during exercise had a normal coronary arteriogram, whereas 11 had evidence of important anatomic coronary artery disease and thus had a false negative echocardlographic findings. Six of these 11 patients had S-T segment depression during exercise. The usefulness of exercise echocardlography to predict coronary artery disease was not altered even when only 26 patients without previous myocardial infarction and with a normal cross-sectional echocardiogram at rest were considered. Thus, new regional wall motion abnormalities during exercise as identified with cross-sectional echocardiography represent a specific finding for the presence of coronary artery disease. However, normal regional wall motion during exercise does not exclude the presence of important anatomic coronary artery disease.     

Increased R-wave amplitude induced by acute myocardial ischemia in the dog: A predictor of malignant ventricular arrhythmias

The ability of an increase of 25 % or greater in the sum of R-wave amplitudes in leads X, Y, Z, L₂, and V₅ to predict the occurrence of malignant ventricular arrhythmias (10 or more ventricular premature beats/min, ventricular tachycardia [5 or more consecutive premature beats], and/or fibrillation) was evaluated in 17 dogs during experimental acute myocardial ischemia. Each dog underwent a 15 minute ligation of the left anterior descending coronary artery followed by reperfusion and after recovery, 2 hours later, a 15 minute ligation of the circumflex coronary artery. During ligation of the left anterior descending coronary artery, 12 of 17 dogs (71%) showed no R-wave increase and no arrhythmias (true-negative response). In 5 (29%) of 17 dogs malignant ventricular arrhythmias developed: 2 of 5 (40%) dogs with arrhythmias had a concomitant R-wave increase (true-positive response), and 3 of 5 (60%) with arrhythmias had a less than 25% increase in R-wave amplitude (false-negative results). During circumflex coronary artery ligation, 13 of 17 (76%) dogs showed both R-wave increases and arrhythmias (true-positive response). Four (24%) of 17 dogs had no arrhythmias: 3 of 4 (75%) with no arrhythmias also had a less than 25% increase in R-wave amplitude (true-negative response), whereas 1 of 4 (25%) dogs with no arrhythmias had an increase in R-wave amplitude (false-positive response). In dogs with both arrhythmias and R-wave increases, R-wave changes preceded the onset of arrhythmias by a mean (± standard deviation) of 1 minute 27 seconds (± 43 seconds). Overall, R-wave increases were highly sensitive (83%), specific (94%), and predictive (94%) for the occurrence of malignant ventricular arrhythmias during experimental acute myocardial ischemia.     

Superior QRS axis of ventricular premature complexes: An additional criterion to enhance the sensitivity of exercise stress testing

The presence or frequency of ventricular premature complexes during exercise is not highly predictive for identifying patients with coronary artery disease. To determine whether the morphologic features or axis of exercise-induced ventricular premature complexes may increase this predictability, a study was made of 63 symptomatic patients with coronary artery disease (electrocardiographic evidence of infarction or occlusive lesions seen on coronary angiography, or both) and 10 control patients with normal coronary arteriograms. In 48 of the 63 patients with coronary artery disease the exercise-induced ventricular premature complexes had a superior frontal plane QRS axis between ?30 ° and ?120 °; in 12 the axis was between ?30 ° and +150 °, and in 2 the axis was indeterminate, between +150 ° and ?120 °. In all 10 control subjects without coronary artery disease the QRS axis of the exercise-induced ventricular premature complexes was in the normal range, between ?30 ° and +150 °. If the standard criterion of 1 mm S-T segment depression were used to predict coronary artery disease during exercise stress testing, 25 of the 63 patients with coronary artery disease would have had a normal or borderline exercise test. However, in 21 of these 25 patients the exercise-induced ventricular premature complexes had a superior axis, a criterion that would enhance the predictive sensitivity of the exercise test from 60 to 94 percent. A left bundle branch block pattern of ventricular premature complexes was not helpful in detecting patients with coronary artery disease, although a right bundle branch block pattern was infrequent in the control subjects. The occurrence of ventricular premature complexes with a superior axis during exercise testing can enhance the exercise test's sensitivity for detecting the presence of coronary artery disease, particularly when this criterion is used in patients with a nondiagnostic S-T segment response to exercise.     

Effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium

The effects of procainamide on strength-interval relations in normal and chronically infarcted canine myocardium were determined in nine adult mongrel dogs susceptible to sustained ventricular tachyarrhythmias. The dogs were studied at 3 to 30 days after two stage occlusion and reperfusion of the mid left anterior descending coronary artery. Unipolar cathodal stimulation (pulse duration 2 ms, drive cycle length 300 ms) was used to evaluate excitability and refractoriness at a total of 19 normal and 22 infarct sites both before and 15 to 30 minutes after intravenous infusion of procainamide, 20 to 25 mg/kg body weight. The electrophysiologic effects of procainamide were evaluated at the time of the plateau phase of procainamide's antiarrhythmic activity in this model. At normal sites, procainamide had only a minimal effect on the mean diastolic excitability threshold (increased from a mean [± standard deviation]of 0.07 ± 0.02 to 0.08 ± 0.02 mA [probability (p) = not significant (NS)], the mean effective refractory period (increased from 137 ± 10 to 139 ± 11 ms [p = NS]) and the mean ventricular refractory period at twice diastolic threshold (increased from 156 ± 12 to 163 ± 16 ms [p <0.01]). At infarct sites, the mean diastolic excitability threshold was similarly unchanged after procainamide (from 0.57 ± 1.13 to 0.57 ± 1.09 mA [p = NS]), but both the mean effective refractory period (from 142 ± 17 to 159 ± 27 ms [p <0.001]) and the mean ventricular refractory period at twice diastolic threshold (from 166 ± 25 to 187 ± 33 ms [p <0.001]) were moderately prolonged. In addition, dispersion of refractoriness between normal and infarct sites as well as within areas of infarcted myocardium was often either unchanged or increased rather than decreased by procainamide.

Thus, the antiarrhythmic activity of procainamide in this canine model of chronic myocardial infarction was not explained by an effect on the excitability or refractoriness of normal myocardium, by changes in the diastolic excitability of infarcted tissue or by an effect on the dispersion of refractoriness. The most prominent effect of procainamide was to decrease the excitability of abnormal myocardium during the relative refractory period and to prolong the refractoriness of abnormal myocardium.     

Apex sector echocardiography in evaluation of the right atrium in patients with mitral stenosis and atrial septal defect.

Cross-sectional echocardiography utilizing the four chamber apical view was used to evaluate right atrial dimensions as a means of detecting abnormal right heart hemodynamics in 20 patients with mitral stenosis, 5 patients with an atrial septal defect and 10 patients without heart disease. Right and left atrial dimensions on apex echocardiography were 40 mm or less in control subjects. There was a good correlation (r = 0.81) between left atrial size assessed with apex sector and M mode echocardiography. In patients with an atrial septal defect, the left atrium was of normal size on apex sector echocardiography; in patients with mitral stenosis, it was larger on apex echocardiography (59 +/- 9 mm) than on M mode echocardiography (51 +/- 8 mm). The right atrium was enlarged (54 +/- 5 mm) on apex echocardiography in all five patients with an atrial septal defect, but the right ventricle was enlarged in only four. Seventeen of 20 patients with mitral stenosis had an enlarged right atrium (53 +/- 7 mm) on apex echocardiography, whereas 15 had normal right ventricular dimensions (21 +/- 9 mm) on M mode echocardiography. Right atrial size on apex echocardiography was enlarged (54 +/- 6 mm) in 10 of 11 patients with mitral stenosis and pulmonary arterial hypertension. Thus, evaluation of the right atrial dimension with apex echocardiography may be more sensitive than M mode echocardiography in detecting early right heart involvement in specific cardiac conditions.     

Role of early cycle ventricular extrasystoles in initiation of ventricular tachycardia and fibrillation: Evaluation of the R on T phenomenon during acute ischemia in a canine model

Eighteen open chest dogs anesthetized with pentobarbital sodium were studied to determine the role of early cycle premature ventricular beats in the initiation of ventricular tachycardia and fibrillation during the initial 30 minutes of acute myocardial ischemia. The coupling interval and prematurity index (R-R′/R-R) of every premature beat after a sinus beat were determined during both the “immediate” (2 to 12 minutes) and “delayed” (13 to 30 minutes) phases of ventricular arrhythmias that follow acute coronary ligatlon. During the immediate phase, characterized by marked fractionation of local electrograms and delayed intramyocardial conduction, early cycle beats were infrequent (8 percent of extrasystoles) and initiated only 3 (4 percent) of 75 episodes of ventricular tachycardia and fibrillation. However, during the delayed phase, characterized by less fractionation and more uniform conduction, early cycle beats were both more frequent (24 percent of extrasystoles, p < 0.001) and more successful (20 [34 percent] of 59 episodes, p < 0.001) in initiating ventricular tachycardia and fibrillation. Thus, the underlying electrophysiologic derangements appeared to be of primary importance in determining both the frequency and relative malignancy of early cycle beats during acute myocardial ischemia.     

Two dimensional echocardiography in mitral, aortic and tricuspid valve prolapse: The clinical problem, cardiac nuclear imaging considerations and a proposed standard for diagnosis

The mitral valve prolapse syndrome may present with a variety of clinical manifestations and has proved to be a common cause of nonspecific cardiac symptoms in clinical practice. Primary and secondary forms must be distinguished. Myxomatous degeneration appears to be the common denominator of the primary form. The diagnostic standard of this form has not previously been defined because the detection of mitral leaflet tissue in the left atrium (prolapse) on physical examination or angiography is nonspecific. M mode echocardiography has greatly enhanced the recognition of this syndrome but has not proved to be the best diagnostic standard because of its limited view of mitral valve motion. The advent of two dimensional echocardiography has provided the potential means for specific identification of the mitral leaflet motion in systole and can be considered the diagnostic standard for this syndrome. Primary myxomatous degeneration with leaflet prolapse is not localized to the mitral valve. Two dimensional echocardiography has detected in preliminary studies tricuspid valve prolapse in up to 50 percent and aortic valve prolapse in about 20 percent of patients with idiopathic mitral valve prolapse.     

Importance of the pacing mode in the initiation of ventricular tachyarrhythmia in a canine model of chronic myocardial infarction

The use of unipolar anodal or bipolar pacing, as compared with unipolar cathodal pacing, purportedly increases the likelihood of inducing inadvertent ventricular fibrillation in susceptible patients. In this study, the ability to initiate sustained ventricular tachycardia or fibrillation with unipolar cathodal, unipolar anodal and bipolar pacing modes was compared using programmed ventricular stimulation at 82 subendocardial periinfarction sites in 11 dogs with chronic myocardial infarction. The late diastolic excitability threshold was significantly higher and the ventricular refractory period was significantly shorter (p less than 0.001) with anodal pacing (mean 0.62 mA, 156 ms, respectively) than with pacing in either the cathodal (0.12 mA, 174 ms) or the bipolar (0.13 mA, 173 ms) mode. At a current intensity twice that of the excitability threshold, the introduction of one or two extrastimuli induced ventricular tachycardia and ventricular fibrillation comparably among the three pacing modes. However, when three extrastimuli were used, ventricular fibrillation was induced with anodal pacing twice as frequently (50 [61%] of 82 sites) as with either of the other two pacing modes (each 23 [28%] of 82 sites, p less than 0.001), whereas the induction of ventricular tachycardia remained comparable with anodal pacing (15 [18%] of 82 sites) and cathodal and bipolar pacing (each 14 [17%] of 82 sites). Furthermore, a similarly high incidence of inducibility of ventricular fibrillation was observed with both cathodal pacing (56 [68%] of 82 sites) and bipolar pacing (40 [49%] of 82 sites) when an increased current equal to twice the anodal excitability threshold (1.23 mA) was used.(ABSTRACT TRUNCATED AT 250 WORDS)     

Tricuspid regurgitation in tricuspid valve prolapse demonstrated with contrast cross-sectional echocardiography

To determine the prevaience of tricuspid regurgitation in patients with tricuspid valve prolapse and to define further the criteria for the diagnosis of tricuspid regurgitation on contrast echocardiography, evaluation was made of 45 patients who had adequate contrast studies. There were four groups of patients: Group A, 10 healthy control subjects with no evidence of structural heart disease on cardiac catheterizattion; group B, 10 patients with classic clinlcal evidence of tricuspid regurgitation; group C, 10 patients with cross-sectional echocardiographic evidence of mitral valve prolapse without tricuspid valve prolapse; and group D, 15 patients with both mitral and tricuspid valve prolapse on cross-sectional echocardiography.Tricuspid regurgitation was sought in each group by using the subxiphoid echocardiographic approach with peripheral venous injection of saline solution. The diagnosis required the presence of microcavitations in both the inferior vena cava and hepatic veins for at least three consecutive cardiac cycles. Tricuspid regurgitation was observed in no patients in group A, 10 of 10 patients in group B, 0 of 10 in groups C and 6 of 15 (40 percent) in group D. Contrast cross-sectional echocardiography proved to be a reliable technique for identifying tricuspid regurgitation with a high degree of specificity and sensitivity. Patients with tricuspid valve prolapse had a 40 percent prevalence rate of tricuspid regurgitation. This finding may identify a subgroup that requires particularly careful clinical follow-up care.