Comparative effects of sodium bicarbonate and sodium chloride on reversing cocaine-induced changes in the electrocardiogram.

Cocaine abuse is associated with a number of cardiovascular complications that include arrhythmias and sudden cardiac death. Although the mechanism(s) remain unclear, cocaine-induced block of sodium channels resulting in slowed cardiac conduction is thought to play an important role. Several reports suggest that the effects of cocaine effects on cardiac sodium channels can be reversed by administration of sodium bicarbonate. Whether the beneficial effects of sodium bicarbonate are due to sodium ions or an increase in blood pH is unknown. Therefore the purpose of this study was to compare the effects of sodium loading alone (by using sodium chloride) versus sodium loading with an associated increase in arterial pH (by using sodium bicarbonate) on reversing cocaine-induced effects on the electrocardiogram (ECG) in a canine model. Seventeen anesthetized dogs received three i.v. injections of cocaine, 5 mg/kg, with each dose separated by 15 min. Two minutes after the third cocaine dose, each dog was randomly assigned to receive 2 mEq/kg i.v. sodium bicarbonate (1 mEq/ml) or 2 mEq/kg i.v. sodium chloride (1 mEq/ml). ECG, electrophysiologic, and hemodynamic data were recorded at baseline, after each cocaine injection, and after administration of sodium bicarbonate or sodium chloride. In both groups of animals, the first cocaine injection significantly (p < 0.05) prolonged the PR, QTc, AH, and HV intervals, and QRS duration compared with baseline. All intervals continued to lengthen in a dose-dependent manner after the second and third cocaine doses. Sodium bicarbonate significantly (p < 0.05) reduced cocaine-induced prolongation of PR [(147 +/- 5-130 +/- 5 ms), AH (81 +/- 6 - 72 +/- 6 ms), and HV intervals (55 +/- 2 - 39 +/- 1 ms). and QRS duration (96 +/- 6 - 66 +/- 4 ms), peak effect after third cocaine dose versus after sodium bicarbonate, respectively]. Sodium chloride had no effect on reversing cocaine-induced effects on the ECG. Cocaine produces dose-dependent slowing of cardiac conduction that is effectively reversed by sodium bicarbonate. The lack of efficacy of sodium chloride suggests that the increase in arterial pH associated with sodium bicarbonate is responsible for reversal of the effects of cocaine on the ECG. Therefore sodium bicarbonate may be clinically useful in the treatment of cocaine-induced cardiac arrhythmias, primarily as a result of its effects on arterial pH.

Right ventricular infarction: specific requirements of management.

The principal cause of right ventricular infarction is atherosclerotic proximal occlusion of the right coronary artery. Proximal occlusion of this artery leads to electrocardiographically identifiable right-heart ischemia and an increased risk of death in the presence of acute inferior infarction. Clinical recognition begins with the ventricular electrocardiographic manifestations: inferior left ventricular ischemia (ST segment elevation in leads II, III and aVF), with or without accompanying abnormal Q waves and right ventricular ischemia (ST segment elevation in right chest leads V3R through V6R and ST segment depression in anterior leads V2 through V4). Associated findings may include atrial infarction (PR segment displacement, elevation or depression in leads II, III and aVF), symptomatic sinus bradycardia, atrioventricular node block and atrial fibrillation. Hemodynamic effects of right ventricular dysfunction may include failure of the right ventricle to pump sufficient blood through the pulmonary circuit to the left ventricle, with consequent systemic hypotension. Management is directed toward recognition of right ventricular infarction, reperfusion, volume loading, rate and rhythm control, and inotropic support.

The comparative predictive accuracy of spectral turbulence analysis and time-domain analysis for sustained monomorphic ventricular tachycardia in postinfarction patients with conduction defects.

Signal-averaged electrocardiograms obtained in 86 postinfarction patients with right bundle branch block (RBBB), left bundle branch block (LBBB), or intraventricular conduction defect (IVCD), underwent time-domain analysis (TDA) and spectral turbulence analysis (STA) to determine which approach provided the more effective marker for patients with sustained monomorphic ventricular tachycardia. TDA parameter included the root mean square value of the last 40 ms of the vectormagnitude complex and the duration of the low amplitude signal below 40 microV. STA utilized a summation lead (X + Y + Z) and quantitated four parameters: interslice correlation mean, interslice correlation standard deviation, low slice correlation ratio, and spectral entropy. High-pass filters of 40 Hz and 25 Hz were used to study the total patient population with noise levels > or = microV and a subset of 67 patients with noise levels < or = 0.5 microV. The techniques compared their effectiveness as measured by their positive predictive values (PPV), negative predictive values (NPV), sensitivity (Sn), and specificity (Sp). In RBBB, STA was uniformly a more powerful tool utilizing either filter at both noise levels. In LBBB, STA was consistently more powerful at both noise levels at 40 Hz and, generally, more powerful at 25 Hz with isolated exceptions. In conduction defects in which QRS was > 100 ms but < 120 ms, TDA was equal to or more effective than STA, with the exception of PPV and Sp at 40 Hz at 1-microV noise level and the Sp at 0.5 microV. The addition of ejection fraction data to STA score resulted in further overall improvement in performance, but above conclusions were unchanged.

Transient loss of sensing and capture during coronary angiography in two patients with permanent pacemakers.

Two cases of transient pacemaker failure to sense and capture during angiography are reported. This phenomenon is due to a transient increase in sensing and pacing thresholds beyond the pacemakers programmed settings. The underlying mechanism may be related to blood displacement, the electrochemical properties of the injectate, the high concentration of the contrast media, or a combination of these properties. Even though the chambers in which sensing and pacing loss occurred differed (ventricle in the first and atria in the second), the episode occurred repeatedly after injection of contrast media into the artery supplying the respective electrode-tissue interface. In pacemaker dependent patients, provisions for external pacing should be implemented prior to injection of contrast into the coronary arteries.

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.

Assessment of late potentials in patients with essential hypertension by the signal-averaged electrocardiogram with five year follow-up.

Both the Framingham and Manitoba Heart Studies have identified electrocardiographic left ventricular (LV) hypertrophy (LVH) as a risk factor for sudden cardiac death. Low amplitude ventricular late potentials in the terminal part of ventricular activation have been associated with sustained ventricular tachycardia and have identified those at risk for sudden cardiac death. Therefore, we prospectively examined 23 essential hypertensives without known symptomatic coronary heart disease by two-dimensional echocardiography and signal averaged electrocardiograms (SAECGs) for the detection of ventricular late potentials. The SAECG vector-magnitude complex measurements included the total duration of the complex (QRSd), the voltage in the last 40 ms (V40), and the duration of low amplitude signals < 40 microV in the terminal portion of the complex (LASd). Echocardiographic parameter means were: LV diastolic diameter = 46.0 +/- 4.5 mm, combined septal and posterior wall thickness = 23.3 +/- 4.2 mm, LV mass (Woythaler method) = 235.1 +/- 69.1 g, LV mass (Penn method) = 199.5 +/- 55.3 g and ejection fraction = 63.9 +/- 6.2%. SAECG measurement means were QRSd = 88.2 +/- 9.9 ms, V40 = 63.1 +/- 34.7 microV RMS, and LASd = 23.5 +/- 10.0 ms. No echocardiographic parameter correlated with SAECG duration; however, age correlated with QRSd (r = 0.48, P = 0.02). Posterior wall thickness (r = -0.43, P = 0.04), LV mass index (r = -0.44, P = 0.03) and LV mass/height (r = -0.49, P = 0.02) inversely correlated with LASd.(ABSTRACT TRUNCATED AT 250 WORDS)

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)

Signal-averaged electrocardiography: history, techniques, and clinical applications.

Signal averaging principles have been utilized since around 1875. Their application in medicine to enhance biologic signals was first made in 1947 for improved detection of electroencephalographic signals. The year 1963 marked the first application of this technique to cardiac signals. The more prevalent use in adult cardiology is in the detection of ventricular late potentials (VLPs) which correspond to areas of delayed ventricular activation as slowed conduction velocity. These VLPs have value in predicting the likelihood of malignant ventricular arrhythmias after myocardial infarction (MI). Negative predictive values on the order of 96-99% are convincing as to their ability to predict no arrhythmic event post-MI. Positive predictive values, on the other hand, are poor (10-29%) but improve (35-62%) in combination with other parameters such as depressed left ventricular function and frequent ventricular ectopy. Additional accepted uses for the signal-averaged electrocardiogram (SAECG) include prediction of successful ablative surgery for intractable ventricular tachycardia and facilitating evaluation of patients presenting with syncope of an unclear etiology. Potential future applications of the SAECG are (1) in following patients for rejection after cardiac transplant, (2) as a screening tool for the need for electrophysiologic study, (3) as a predictor of vessel patency after thrombolysis or percutaneous transluminal coronary angiography, and (4) as a tool to assess proarrhythmia. As the technique of signal averaging continues to evolve, its applications may become more diverse and its clinical effectiveness may improve.

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.

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.

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.

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.

Application of beat-to-beat techniques.

The focus of this report is to describe a system for recording surface His-Purkinje and ventricular late potentials on a beat-by-beat basis outside of a shielded environment. An AC magnetic field monitoring device was designed for improved site selection, orientation, and quality control of the acquisition. His-Purkinje signals are detected utilizing spatial averaging and specific channel selection algorithms applied to discriminate random noise from signal. Beat-by-beat vectormagnitude complexes were generated from pairs of X, Y, and Z leads. Both infinite impulse response (IIR) filters, modified for beat-by-beat approaches, and finite impulse response (FIR) filters were utilized. Using the IIR filter, beat-by-beat recordings from test subjects were compared to the signal averaged electrocardiogram (SAECG). Measurement parameters from normal test subjects fell within the previously specified normal range for the SAECG. The IIR filter applied to beat-by-beat recordings exhibited sharp frequency response and a precisely defined cutoff frequency allowing maximal attenuation of the low frequency components in the ST segment. While filter ringing was eliminated, discontinuity and distortion of the filtered waveform resulted. The FIR filter with linear phase response retained the integrity and morphology of the complex but because of its flat frequency response, the ST segment was not as well attenuated and it was more difficult to isolate late potentials. A high order FIR filter should be used if the desire is to match the frequency response of the four-pole IIR filter, since the frequency response of the FIR filter is primarily determined by the order of the filter.(ABSTRACT TRUNCATED AT 250 WORDS)

Possible triggering of paroxysmal atrial fibrillation in normal hearts by psychological stressors: a report of two cases.

Paroxysmal atrial fibrillation was triggered by psychological stress in two patients, both of whom had normal echocardiograms and coronary angiography. Neither patient was alcoholic or had ingested ethanol in relation to the onset of atrial fibrillation and both were free of metabolic derangements. Possible mechanisms involved in the triggering of atrial fibrillation are discussed.

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.

Patterns of body surface potential and ventriculograms specific to occlusion of subdivisions of the coronary arteries.

The thoracic activation map patterns, the distribution of occlusions, and the ventriculograms obtained at cardiac catheterization were examined in 166 patients with multivessel coronary disease without conduction defects or prior coronary intervention. The mean potential and ventriculographic configurations were determined for 15 groups, each formed on the basis of significant luminal occlusion (less than or equal to 90%) of an individual coronary arterial subdivision. We mathematically extracted distinctive map and wall motion patterns specific for isolated occlusion of each of the 15 major subdivisions. For these prototypes we found the following: 1) Definitive change in electrical pattern (less than 2 SD from the normal mean) occurred frequently outside the electrode sites of the standard electrocardiogram. 2) Focal akinesis systematically followed lesion site down the arterial courses; early electrical activation patterns corresponded to identifiable anatomic loss. 3) Certain paradoxes arose, for example, similar wall motion change but quite dissimilar electrical patterns from posterior descending artery occlusion of right coronary versus left circumflex origin. This technique unmasks component surface electrical patterns and ventriculographic deformities otherwise unrecognized in multisite, multivessel disease.