Left bundle branch block: a continuously evolving concept.

Eppinger and Rothberger in 1909 and 1910 first acknowledged the importance of the conduction system, yet a confusion of the pattern of left bundle branch block with right bundle branch block resulted which persisted for 25 years. In left bundle branch block, right ventricular endocardial activation begins before, and is often completed before, initiation of left ventricular endocardial activation. Most likely, right to left septal activation then follows, resulting in left ventricular endocardial activation. Although it is hazardous to make definitive diagnoses of infarction in the presence of left bundle branch block, clues do exist. Benign left bundle branch block is rare; usually disease becomes manifest. Electrocardiographic criteria of hypertrophy are not as helpful in older patients with chronic left bundle branch block (mainly because of the very high incidence of left ventricular hypertrophy) as in younger patients with block of nonatherosclerotic origin. Left bundle branch block is often associated with other abnormalities of the conduction system. Fascicular blocks may mask or mimic myocardial infarction. Left posterior fascicular block is most often an indicator of left ventricular myocardial deficit if right ventricular enlargement is eliminated. Mortality is higher in patients with associated left axis deviation than in those with a normal axis, although the incidence of progression of atrioventricular (AV) block is low. In symptomatic patients with prolonged His to ventricular intervals, the incidence of progression of AV block is higher (12%). Preexisting left bundle branch block in the absence of clinical evidence of heart disease is rare, yet carries with it a slightly increased mortality. Newly acquired left bundle branch block carries a 10-fold increase in mortality; the incidence of sudden death as the first manifestation of heart disease is increased 10-fold.

Analysis of PR subintervals in normal subjects and early studies in patients with abnormalities of the conduction system using surface His bundle recordings.

Utilizing several different approaches to noise reduction, satisfactory beat by beat His bundle activity was recorded from the chest surface in 41 (80%) of 52 normal subjects. Surface atrial to His intervals (PAH) and His to ventricular intervals (HV) were measured in this group and compared with subintervals of the PR segment recorded endocardially from 47 persons with normal electrophysiologic findings. A recent modification in the selection algorithm allows on-line identification of the four of five possible recording sites for utilization in a spatial summation. The ability to record in less favorable circumstances has been improved to the extent that records of suitable clarity for measurement were also obtained in 17 (77%) of 22 individuals with conduction system abnormalities. Comparison of the surface and endocardially acquired data in the normal group reveals no statistically significant difference in the surface acquired PAH and endocardially acquired high right atrial to His (HRAH) intervals, nor in the HV intervals. In a small subset of patients data were acquired by both techniques and no significant differences were found. Thus, when programmed stimulation or endocardial mapping is not required to answer specific clinical questions, in the majority of persons it is possible to record meaningful subintervals from the body surface from each cardiac cycle. Additionally, in instances in which surface P wave activity is obscure in the routine electrocardiogram, this technique enhances atrial electrical activity.

Racial differences in myocardial ischemia and coronary flow reserve in hypertension.

OBJECTIVES: Using invasive measurements of endothelium-independent coronary flow reserve and stress thallium testing with or without dipyridamole, this study investigated racial differences in ischemia and coronary reserve in hypertensive left ventricular hypertrophy. BACKGROUND: African Americans compared with Caucasian Americans appear to have a higher case fatality from coronary heart disease but lesser amounts of atherosclerotic coronary artery disease. This paradox may be explainable by intrinsic or acquired racial differences in coronary arteriolar autoregulation and vasoreactivity. METHODS: The study enrolled 91 African and 81 Caucasian Americans referred for cardiac catheterization because of suspected myocardial ischemia but found to have no significant coronary stenosis. Patients were stratified by degree of left ventricular hypertrophy for comparison purposes after calculation of indexed left ventricular mass by means of echocardiographic M-mode measurements. Coronary flow reserve measurements were made using the intracoronary Doppler catheter and hyperemic doses of intravenous dipyridamole in 100 patients and intracoronary papaverine and adenosine in 72 patients. Seventy-seven percent of patients underwent adequate stress thallium testing with or without dipyridamole. RESULTS: In African Americans, mean (+/- SD) coronary flow reserve decreased from 4.4 +/- 2.3 for 38 without mass hypertrophy to 3.2 +/- 1.3 for 53 with hypertrophy (p = 0.005) to 2.7 +/- 1.1 for 12 with severe hypertrophy (p = 0.02). Thallium testing was abnormal in 31% of those without mass hypertrophy and 59% of those with hypertrophy. In Caucasian Americans, coronary flow reserve decreased from 4.1 +/- 2 for 58 without hypertrophy to 3.6 +/- 1.5 for 23 with hypertrophy (p = NS) to 3 +/- 1.5 for 6 with severe hypertrophy (p = NS). Thallium testing was abnormal in 36% without mass hypertrophy and in 39% with hypertrophy. CONCLUSIONS: This study establishes that development of left ventricular hypertrophy in hypertension carries greater physiologic morbidity for African compared with Caucasian Americans, typified by marked reduction in endothelium-independent coronary flow reserve and increased frequency of abnormal thallium tests.

Standards for analysis of ventricular late potentials using high-resolution or signal-averaged electrocardiography: a statement by a task force committee of the European Society of Cardiology, the American Heart Association, and the American College of Cardiology.

Sufficient data are available to recommend the use of the high-resolution or signal-averaged electrocardiogram in patients recovering from myocardial infarction without bundle branch block to help determine their risk for developing sustained ventricular tachyarrhythmias. However, no data are available about the extent to which pharmacological or nonpharmacological interventions in patients with late potentials have an impact on the incidence of sudden cardiac death. Therefore, controlled, prospective studies are required before this issue can be resolved. As refinements in techniques evolve, it is anticipated that the clinical value of high-resolution or signal-averaged electrocardiography will continue to increase.

ACC policy statement. Recommended guidelines for training in adult clinical cardiac electrophysiology. Electrophysiology/ Electrocardiography Subcommittee, American College of Cardiology.

Training in clinical cardiac electrophysiology should take place in an Accreditation Council for Graduate Medical Education accredited cardiology program, and the electrophysiology training program itself should be accredited by the Council. Each trainee must be eligible for board certification in Internal Medicine and either eligible for certification in Cardiovascular Diseases or in a program leading to eligibility. Training faculty should be certified in clinical cardiac electrophysiology or demonstrate equivalent credentials. At least two training faculty members are preferred. The faculty must be dedicated to teaching, active in performing or promoting research and must spend a substantial portion of their time in research, teaching and practice of clinical electrophysiology. A curriculum of training should be established. Faculty experts in the related basic sciences should be available and involved in teaching. The institution should have a fully equipped clinical electrophysiology laboratory and complete noninvasive capabilities. A close working relation with a cardiac surgery faculty member skilled in surgical treatment of arrhythmias is required. Training in application of pharmacologic and all current nonpharmacologic therapies, in the outpatient and inpatient setting, is necessary. The clinical exposure must include all facets of arrhythmia diagnosis and treatment and must be quantitatively sufficient to allow the trainee to develop proficiency. The period of training should not be less than one year in addition to the period of cardiology fellowship required by the ABIM for board eligibility. A continuous period of training is preferred.

Leukocyte ascorbic acid and its relationship to coronary artery disease in man.

The ascorbic acid level of the leukocytes in patients with coronary artery disease was compared to the ascorbic acid level of the leukocytes in patients without coronary artery disease as demonstrated by coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary arteriography. The leukocyte ascorbic acid level was found significantly lower in patients with coronary atherosclerosis (P < 0.001). There was also significant difference in the leukocyte ascorbic acid levels among patients with abnormal coronary arteriograms who smoked compared to those who did not. The anatomical changes secondary to atherosclerotic disease, and mainly those changes related to the ground substance, have been shown to be the changes that have been observed in patients with ascorbic acid deficiency. From the present study, with its limitations, it is suggested that ascorbic acid may play a role in the pathogenesis of atherosclerosis, and although not implicated as an etiological factor in coronary artery disease, it suggests that a closer look at its possible role in the pathogenesis and progression of coronary artery disease is warranted.

Treatment of torsades de pointes with esophageal atrial pacing.

A 65-year-old woman presented with new onset atrial fibrillation. Medical therapy with digoxin and quinidine was not effective in controlling the arrhythmia. Subsequently, complications developed including a stroke and torsades de pointes. The arrhythmia was successfully controlled by overdrive suppression by esophageal pacing. This case illustrates the usefulness of esophageal pacing and how it may be applied in emergencies when transvenous pacing cannot be readily performed outside the intensive care unit setting.

Posterior fascicular block versus posteroinferior myocardial infarction in left posterior excitation disturbances.

To delineate electrocardiographic similarities and differences in ventricular depolarization between left posterior fascicular block and posteroinferior myocardial infarction, these lesions were produced in two and three stage experiments in dogs and baboons. The observed QRS changes of left posterior fascicular block were found to be immediate, little influenced by healing of the acute lesion, and partially correctable by pacing viable myocardium distal to the block. In contrast, the QRS changes of posteroinferior myocardial infarction occurred later with cicatrization and were essentially unaffected by pacing. The intrinsic deflection in direct posterior epicardial leads was more delayed by left posterior fascicular block than by posteroinferior myocardial infarction. Both lesions accounted for Q waves in leads II, III and aVF. However, R amplitude in these same leads was increased after left posterior fascicular block but decreased after posteroinferior myocardial infarction. The mean QRS axis in the frontal plane was shifted toward the vertical in left posterior fascicular block but little changed or shifted slightly away from the vertical in posteroinferior myocardial infarction. When left posterior fascicular block and posteroinferior myocardial infarction coexist, there may be masking, imitation or enhancement of the effects of one lesion by the presence of the other. To assist in recognition, distinguishing features are described.

Late potentials in normal subjects and in patients with ventricular tachycardia unrelated to myocardial infarction.

Fifty normal male and female athletes, or athletically active subjects, were evaluated, and a search for low-amplitude late potentials in the terminal part of ventricular activation was performed. Recordings from 3 normal men met the definition of abnormal late potentials, and were indistinguishable by present analytic techniques from those encountered in patients who have ventricular tachycardia (VT) after myocardial infarction (MI). Of 24 patients studied, 11 had VT, but only 2 had had an MI, which occurred in the remote past. Another patient had 1 narrowed coronary artery on arteriography. Group differences could be demonstrated using amplitudes and durations of late potentials, but late potentials generally did not prove the impressive marker of the patient with VT, which other workers, as well as ourselves, have encountered in patients after MI. Late potentials were an impressive marker in a subset of the VT group in whom cardiomegaly developed. Thus, the absence of late potentials is an effective marker in the normal subject, but the presence of late potentials is not an effective marker in identifying the patient with non-MI-related, nonsustained VT before development of cardiomegaly.

Effect of left ventricular aneurysm on risk of sudden and nonsudden cardiac death.

Although left ventricular (LV) aneurysm is associated with increased mortality, its independent prognostic significance is controversial. To determine the effect of LV aneurysm on risk, 121 patients with healed myocardial infarction (MI), 55 manifesting akinesia on ventriculography (MI group) and 66 with LV aneurysm characterized by diastolic deformity (eccentricity) and systolic dyskinesia (LV aneurysm group) were studied. At a mean follow-up of 5.7 years, there were 32 cardiac deaths (12 MI vs 20 LV aneurysm), including 9 sudden deaths (1 MI vs 8 LV aneurysm). Multivariate analysis revealed decreasing ejection fraction to be the best predictor of total cardiac death, and revascularization to be protective. Nonsudden cardiac death was predicted by ejection fraction, absence of revascularization and right coronary artery disease, whereas sudden cardiac death was predicted by LV aneurysm and the frequency of ventricular ectopic complexes on Holter monitoring. In the MI group, ejection fraction was the only significant predictor of total cardiac death and nonsudden cardiac death. In the LV aneurysm group, total cardiac death, as well as nonsudden cardiac death, were predicted by ejection fraction, ventricular tachycardia and right coronary artery disease, whereas ventricular tachycardia predicted sudden cardiac death. It is concluded that the risk profile for total cardiac death differs between LV aneurysm and MI patients, and that LV aneurysm constitutes an independent predictor of late sudden cardiac death after MI. Moreover, on a substrate of LV aneurysm, the risk factors for sudden cardiac death and nonsudden cardiac death differ, with ventricular tachycardia being the sole predictor of sudden cardiac death. Furthermore, Holter monitoring is valuable in identifying patients at persistent risk of sudden cardiac death.

The degree to which myocardial infarct site and size determine the electrocardiographic axis. Analysis of correlative data by computational modeling.

The spatial electrical QRS axis was determined for 428 twelve-lead electrocardiograms from patients subsequently shown by postmortem dissection to have ventricular myocardial fibrosis or necrosis. Four 16-segment ventricular models of the heart were used to "predict" the spatial electrical QRS axis from known ventricular mass and deficit. The raw model I in ideal anatomic position and vectors perpendicularly outward for each muscle segment showed a mean correlation value of -0.494; model II was rotated in the chest to produce best fit with a correlation of 0.638, but the anatomic orientation was not reasonable; model III maintained original position and orientation but the vectors were scaled (correlation 0.780); and model IV, with nonperpendicular vectors, yielded a mean correlation of 0.793. The exceptions to good predictability formed a distinct subset largely composed of electrocardiograms with some form of variant intraventricular conduction (slight QRS widening, fascicular block patterns and "indeterminate frontal-plane axis").

Effect of various regimens of chronic and acute nicotine exposure on myocardial infarct size in the dog.

Smoking is a risk factor for atherosclerotic coronary heart disease, and the risk increases with increasing numbers of cigarettes smoked. The effect of cigarette smoking on the size of acute myocardial infarction (AMI) has not been evaluated. This study describes the effect of 1 component of tobacco smoke, nicotine, on the size of experimentally induced AMI in closed-chest dogs. Daily exposure to nicotine before AMI increased the volume of infarcted tissue (p less than 0.0001). Acute exposure to nicotine (with prior chronic exposure) resulted in a larger volume of infarcted tissue (p less than 0.0001). Thus, chronic, acute and post-AMI exposure to nicotine has an adverse effect on the volume of subsequent infarcted tissue, and continued exposure after AMI further enlarges infarct size.

New evidence for inferoposterior myocardial infarction on surface potential maps.

Extensive body surface potential recording was performed in 22 patients 2 to 4 weeks after an acute inferoposterior myocardial infarction. Serial isometric projection maps were viewed millisecond by millisecond throughout ventricular excitation, and a second series of maps were examined after removal of the expected range of normal potential distribution. Three major findings outside the normal range appeared: (1) In 6 patients, an early zone of abnormal positivity developed in the left anterior chest at xiphoid level between 15 and 30 msec after onset of the QRS complex; (2) in 13 other patients, a large zone of positivity developed high on the left anterior chest (subclavicular region) between 30 and 60 msec after QRS onset; and (3) in 8 patients the long-lasting rim of negativity about the lower chest was strictly abnormal compared with the expected range. Thus, in 19 of 22 patients the potential map expression was outside the normal range, whereas only eight standard electrocardiograms revealed persistent Q waves with a duration greater than 30 msec. We believe the mid and late activation changes are related to ischemically induced alterations in the temporal sequence of ventricular excitation, not easily appreciated by conventional means of recording but obvious with the departure map technique.

Morphologic, hemodynamic and coronary perfusion characteristics in severe left ventricular hypertrophy secondary to systemic hypertension and evidence for nonatherosclerotic myocardial ischemia.

Patients with the clinical diagnosis of ischemic heart disease who were found to be free of significant coronary artery atherosclerotic disease (n = 150) underwent coronary vasodilator reserve testing, 2-dimensional echocardiography, and dipyridamole limited-stress thallium testing. After exclusions (predominantly for technically poor coronary artery Doppler signals or suboptimal echocardiography), 100 patients formed the study population. The purpose was to characterize typical cardiac and coronary artery findings in hypertensive patients with severe left ventricular (LV) hypertrophy (n = 15) and to investigate the evidence for myocardial ischemia unrelated to coronary atherosclerosis in early and advanced hypertensive heart disease. Normotensive and hypertensive control groups without LV hypertrophy (n = 12 and 34, respectively) were used for comparison. Severe LV hypertrophy was defined as LV mass index greater than or equal to 50% above established gender specific norms using 2-dimensional-directed M-mode echocardiography and the cube equation corrected to agree with necropsy estimates of mass. Clinical characteristics more often associated with severe LV hypertrophy were black race (67%), diabetes mellitus (33%), proteinuria (47%) and elevated creatinine (1.5 +/- 0.9 mg/dl). Baseline electrocardiograms and dipyridamole limited-stress thallium scans were highly likely to be abnormal (94 and 73%, respectively). Both eccentric and concentric cardiac hypertrophies were found in the severe group. Ejection fraction was significantly lower (0.51 vs 0.68, p = 0.002) and basal coronary flow velocity higher (12.0 vs 5.0 cm/s, p = 0.0004) among these patients when compared with normotensive control patients. Coronary flow reserve did not differ between control groups but was significantly depressed in patients with severe LV hypertrophy (2.5 vs 3.9, p = 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Relation of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction.

This study explores the relation of the presence of peri-infarction block to ventricular late potentials in patients with inferior wall myocardial infarction (MI). The hypothesis was that both the gross peri-infarction block pattern and subtle low-level ventricular late potentials are expressions of conduction abnormality associated with infarction. The consequent question arose whether peri-infarction block may have the same association with sustained ventricular arrhythmias that has been demonstrated in postinfarction patients with ventricular late potentials. Seventy patients with documented Q-wave MI were divided into those with (23) and those without (47) peri-infarction block. Signal-averaged electrocardiograms were obtained. Analysis of the vectormagnitude complex revealed that the total duration of that complex and the duration of terminal potential under 40 microV in the peri-infarction group exceeded that in the group without peri-infarction block (p less than 0.0001). The voltage in the last 40 ms of the vectormagnitude complex was also significantly less in the peri-infarction group (p less than 0.0005). There were 13 instances of sustained ventricular tachycardia, ventricular fibrillation or sudden death occurring subsequent to infarction not associated with the acute ischemic event, 11 of which occurred in the peri-infarction group. The significantly higher incidence of late potentials along with the significantly higher incidence of sustained ventricular arrhythmias in the peri-infarction block on the surface electrocardiogram may provide another marker for identifying persons at increased risk for these arrhythmias subsequent to MI.

Relation between the ventriculographic silhouette and topography of thoracic potential in coronary artery disease.

The body surface potential map obtained within 30 days of cardiac catheterization was examined in 180 patients with coronary artery disease. Radii to the systolic and diastolic boundaries of the right anterior oblique ventriculogram were measured at 18 degrees intervals; isointegral voltages were tabulated for early and late halves of the QRS complex at 35 definitive electrode sites. Multivariate analysis showed all ray lengths depended on all 70 voltage values. Linear transformation matrices to predict ray length from voltage distribution were calculated for a training set which was successively expanded from 80 to 160 at increments of 20 patients. Training set expansion led to a progressive decrease in the error of reproduction of the ray lengths for patients outside the training set. There is a strong relation between ventriculographic contours in patients with coronary artery disease and body surface potential values during early and late QRS complexes. Even in simplified linear formulation, the relation is detectable throughout a large population despite interindividual variations in anatomic geometry.

ECG changes in hypothermia from sepsis and unrelated to exposure.

The patient had classic ECG changes of hypothermia (sinus bradycardia, prolonged PR interval, prolonged QT interval, and Osborn waves). These changes occurred in hypothermia resulting from sepsis, without exposure being a factor. Documentation of Osborn waves in this clinical setting supports the theory that they result as a direct consequence of myocardial cooling.

Echocardiographic features of flail aortic valve.

This patient had an attack of subacute bacterial endocarditis involving the aortic valve. He developed fulminating congestive heart failure secondary to acute aortic regurgitation, terminating in the prosthetic replacement of his aortic valve. The echo from the aortic valve demonstrated marked coarse fluttering of the cusps, both in systole and in diastole. The two cusps did not coapt in diastole. The echo from the mitral valve showed features of acute regurgitation. The carotid pulse tracing showed marked slurring in its descending limb. The postoperative echocardiogram showed absence of these findings. We suggest that a diagnosis of flail aortic valve be considered in patients suffering from significant isolated aortic regurgitation in the absence of calcification of the aortic valve and with a negative VDRL test for syphilis.

Echocardiographic diagnosis of a stuck Bjork-Shiley aortic valve prosthesis.

A 55-year-old man who had been asymptomatic after replacement of his aortic valve with a Bjork-Shiley prosthesis, suddenly developed heart failure. The clinical suspicion of prosthetic malfunction was not only confirmed, but specified as being a stuck disc secondary to a large thrombus. Surgical removal of the clot resulted in restoration of normal function and return to the expected findings on echocardiogram. The value of echocardiography in such instances, as well as in routinely following-up patients with prostheses postoperatively, is emphasized.

Surgical treatment of thrombosed Björk-Shiley aortic valve prosthesis.

Massive thrombosis of a Björk-Shiley aortic valve prosthesis occurs with significant frequency when adequate anticoagulation has not been attained. The converse is also true: This complication is extremely rare in patients receiving anticoagulant therapy. Therefore, we recommend anticoagulants for all patients with Björk-Shiley aortic valve prostheses. Once a diagnosis of a thrombosed prothesis is made, however, immediate operation is indicated. Declotting of the valve without removal of the disc is adequate treatment. After thrombectomy, it is extremely important to evaluate the entire prosthesis critically, with particular attention to the area of the hinge and the occluder. If any wear is observed, the entire prosthesis should be replaced. Excellent long-term results can be expected if the patient is maintained on adequate anticoagulation postoperatively.