U wave: facts, hypotheses, misconceptions, and misnomers.

The clinical significance of U wave is limited to the occasional obfuscation of the end of T wave and an inadequately explained U wave inversion associated with myocardial ischemia, infarction, and ventricular hypertrophy and dilatation. Lengthening of QT interval often interferes with the recognition of U wave. The characteristics of U wave are not compatible with the Purkinje or ventricular muscle repolarization hypotheses. The timing of the U wave during ventricular relaxation and the links between U wave and mechanical events favor the mechanoelectrical hypothesis of U wave genesis. Unfortunately, little research has been done to test this hypothesis.

Reversible QRS changes during acute myocardial ischemia.

Reversible QRS complex changes associated with ST-segment shift during acute myocardial ischemia (AMI) have been reported sporadically in isolated cases or in small patient groups but have not been analyzed systematically in a sizable cohort of patients. During the past 4 years, a purposeful search was made for electrocardiograms with documented reversible QRS changes associated with all acute injury pattern. The measured variables included distribution of leads with ST-segment deviation and reciprocal ST-segment depression, magnitude of the ST-segment shift, amplitude and direction of the initial and terminal QRS deflections, QRS duration, QTc duration, and U wave amplitude. Reversible QRS changes encountered in 29 patients with AMI included new Q waves (n = 3), decreased Q amplitude (n = 2), QS change to qRS or qR (n = 6), disappearance of QS or Q (n = 4), increased R amplitude (n = 9), decreased R amplitude (n = 6), increased S amplitude by more than 75% (n = 18), and increased QRS duration (n = 4). Changes in the initial configuration were present in 24 of the 29 patients. Reversible changes of the terminal QRS portion occurred in all 29 patients, and reversible changes of the initial QRS portion occurred in 23 (79%), whereas QRS duration increased in 4 patients. Reversible QRS changes during AMI are attributed to passive pull by the ST-segment shift and intraventricular conduction disturbance.

QRS changes during percutaneous transluminal coronary angioplasty and their possible mechanisms.

OBJECTIVES: The purpose of the study was to describe the configuration, and investigate the mechanisms, of QRS changes occurring during percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: QRS changes during PTCA have been attributed to both a passive ST segment shift and conduction disturbances (peri-ischemic block). The direct relation between ST segment shift and QRS changes, however, has not been established, and the definition of conduction disturbances remains to be clarified. METHODS: Twelve-lead electrocardiograms (ECGs) were recorded before PTCA, at the end of 2 min of PTCA and after return to baseline values in 29 patients (left anterior descending coronary artery [LAD] in 13 patients, right coronary artery [RCA] in 14 and left circumflex coronary artery in 2). Electrocardiographic complexes before and during PTCA were superimposed to determine the amplitudes of initial, terminal and total QRS deflection; the relations of QRS changes to baseline (TP segment) and ST segment shift; and the duration of QRS and corrected QT intervals. RESULTS. 1) The direction of the initial QRS deflection was unchanged, but changes of its amplitude occurred. 2) Terminal QRS deflection changed in all patients with a ST segment shift > 17% of the R amplitude, and the correlation between the decrease in the S amplitude and ST segment shift was significant (r = 0.9, p < 0.01) in patients with LAD PTCA. Correlation between changes in total QRS amplitude and ST segment shift in patients with RCA PTCA was weaker (r = 0.54, p = 0.056). 3) Transient conduction disturbance manifested by QRS widening in selected leads occurred in 2 of 29 patients. CONCLUSIONS. 1) Changes in terminal QRS deflection during PTCA are proportional to the magnitude of the ST segment shift. 2) Conduction disturbances manifested by increased QRS duration occurred infrequently. We suggest that the term peri-ischemic block be applied only to changes in QRS configuration associated with QRS widening.

Will QT dispersion play a role in clinical decision-making?

(1) Dispersion of QT intervals is the difference between the longest and the shortest QT interval in the ECG. Owing to the relative ease of measurement and the perceived need for new markers of arrhythmogenicity, the method has attracted the interest of clinical investigators but has not reached the level of practical utility. (2) It is postulated that to pass the test of practical utility, the method must meet the following criteria: (a) standardization; (b) establishment of normal values; (c) established sensitivity and/or specificity for diagnosis and/or prognosis; and (d) uniqueness of relevant information. (3) Analysis of the data from the literature suggests that standardization of the method and the range of normal values have not been established, and that the method lacks specificity for separating healthy persons from patients with heart disease. (4) Large values, such as average QT dispersion > 65 msec, have been found predominantly in patients with serious, life-threatening ventricular tachyarrhythmias, and the largest values, i.e., > 110 msec in patients with congenital long QT syndrome. (5) The prognostic value of QT dispersion has been disputed, and the uniqueness of the relevant information has not been tested. (6) It is concluded that the acceptance of QT dispersion as a useful test in practice faces manifold and serious obstacles. It remains to be established whether these obstacles are insurmountable.

Prognosis of patients with frequent premature ventricular complexes and nonsustained ventricular tachycardia after coronary artery bypass graft surgery.

BACKGROUND: Previous studies in small groups of predominantly nongeriatric patients showed that complex ventricular arrhythmias occurring after coronary artery graft (CABG) surgery are of no prognostic significance. The purpose of this study was to compare the prognosis of patients with and without advanced grade ventricular arrhythmias (AGVA) after CABG in a large group of patients. [In this paper, AGVA is used as an abridged definition of frequent premature ventricular complexes (PVCs) and nonsustained ventricular tachycardia (NSVT) which represent advanced grade ventricular arrhythmias.] METHODS: Twenty-four hour ambulatory electrocardiographic (ECG) monitoring was performed 3 days after CABG in 185 consecutive patients with 185 closely matched control patients without AGVA. Of 185 patients with AGVA, 77 had frequent PVCs, 45 had NSVT, and 63 patients had both. The average age of both groups was 65 +/ 9.7 years. Patients were followed for 34 +/ 10 months, and in 30 patients ambulatory monitoring was repeated at the end of the follow-up. RESULTS: Fifteen AGVA and nine control patients died. In each group seven deaths were noncardiac. Six nonsudden and two sudden cardiac deaths (SCD) occurred in the AGVA group at 2-36 months after CABG and two nonsudden cardiac deaths in the control group at 3 and 35 months after CABG (p = 0.053). Both SCDs occurred 33 months after CABG after new events known to predispose to SCD. In 18 of 30 patients AGVA was no longer present when ambulatory ECG monitoring was repeated 36 +/ 11 months after CABG. CONCLUSION: AGVA after CABG was not a marker of an early sudden cardiac death. In 60% of patients not treated with antiarrhythmic drugs, AGVA was no longer present late after operation.

Transient T wave abnormalities after cessation of ventricular preexcitation: memory of what?

(1) Ventricular preexcitation causes both secondary and primary T wave changes. The secondary changes disappear immediately after cessation of preexcitation (ablation of accessory pathways) and unmask the primary T wave changes that regress within days, weeks, or months. (2) The pattern of primary T wave change produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections and deviation of the T wave vector superiorly. The left lateral connections are associated with rightward deviation of the T wave vector in the frontal plane. (3) The primary T wave abnormalities are believed to be caused by local lengthening of repolarization, but the site of the postulated abnormalities needs to be established. (4) The persistence and slow dissipation of the primary T wave change induced by ventricular pacing, left bundle branch block, and presumably ventricular preexcitation have been attributed to the memory of past events. The nature of these events is not known. Several in vitro models demonstrated phenomena of gradual adjustment of ventricular action potential duration to change in cycle length, or to altered pattern of stimulation, but none of such models has mimicked the long-lasting regression of T wave abnormalities. (5) The terms T wave memory and pseudoprimary repolarization changes lack specificity and are unnecessary additions to the electrocardiographic vocabulary.

The enigma of sudden cardiac death related to dieting.

The use of liquid protein products for treatment of obesity in the United States in the 1960s and '70s was associated with an increased risk of sudden cardiac death. The latter was related to long QT interval occurring in the absence of structural abnormalities of the heart. In an attempt to increase understanding of this phenomenon, the authors examined the possible role of diet-related circumstances. No evidence of increased incidence of sudden cardiac death or significant lengthening of QT interval in obesity, weight loss, starvation and dieting by methods other than liquid protein intake were found. It was concluded that sudden cardiac death during use of liquid protein products remains an enigma, but that other methods of properly medically supervised dieting appear to be safe.

Cycle length-dependent action potential duration and contractile force at various [Ca2+]o in guinea pig papillary muscle.

This study was designed to determine the role of calcium in the cycle length-dependent changes in the action potential duration (APD) and the contractile force in guinea pig papillary muscle. APD correlated with the contractile force during the steady state, with [Ca2+]o ranging from 0.3-7.2 mM. High [Ca2+]o increased the force and shortened APD, while low [Ca2+]o had the opposite effect. During the steady state, as the cycle length of stimulation was decreased, the increase in the contractile force was inversely related to the increase in APD within a [Ca2+]o range of 0.9-5.4 mM and at diastolic intervals of < or = 600 msec. At longer diastolic intervals, the relationship between changes in contractile force and changes in APD was variable and non-linear at each [Ca2+]o. Changes in the postextrasystolic force were not related to APD. The phenomenon of APD overshoot i.e., an APD that was longer during short than during basic cycles, was observed at < 5.4 mM [Ca2+]o and was most pronounced at the lowest [Ca2+]o. Assuming that the contractile force reflects [Ca2+]i, we concluded that the cycle length-dependent APD curve during the steady state is influenced by [Ca2+]i in a manner consistent with the inverse relationship between APD and the contractile force.

Role of potassium channels in cycle length dependent regulation of action potential duration in mammalian cardiac Purkinje and ventricular muscle fibres.

This review examines the putative role played by three repolarising potassium currents, namely the transient outward current (ito), the inward rectifying current (iK1), and the late outward rectifying current (iK), in the regulation of action potential duration in cardiac Purkinje and ventricular muscle fibres under normal physiological conditions. The role of other potassium currents, including the ATP activated current (iK,ATP) under these conditions is uncertain. Personal experiences and work of others are reviewed to summarise: (1) regulation of normal cycle length dependent action potential duration: (2) the characteristics of ito, iK1, and iK pertinent to repolarisation; and (3) the effects of potassium channel blockers and activators on cycle length dependent action potential duration. The presence of ito creates a notch after depolarisation and limits action potential duration at long cycles. Block of iK1 prolongs action potential duration predominantly by slowing phase 3 of the action potential. Block of iK prolongs the duration predominantly by lengthening phase 2 of the action potential, and the lengthening becomes more pronounced at longer cycles. Activation of iK,ATP shortens the duration, and the shortening becomes more pronounced at longer cycles. Each of the three major repolarising potassium currents appears to play a different role in modulating the action potential duration. Ito creates a notch which resets the early course of plateau, and also limits the duration at long cycles. IK1 contributes to maintenance of plateau and controls repolarisation course during phase 3 of the action potential. IK plays major role in controlling action potential duration within a wide range of cycle lengths in Purkinje fibres, and when present, also in ventricular muscle fibres.

Familial congenital sinus rhythm anomalies: clinical and pathological correlations.

We describe pathological abnormalities in a 72-year-old male member of a family with a congenital absence of sinus rhythm and a tendency to develop atrial fibrillation at an early age, and in a 54-year-old female member of a family with cardiomyopathy and progressive conduction system disease manifested by first-degree atrioventricular (AV) block, left bundle branch block, and atrial arrhythmias. Both patients died suddenly. The absence of sinus rhythm in case 1 could be explained by marked atrophy, degeneration, and isolation of the sinoatrial (SA) node. The SA node was also diseased in the member of the other family with atrial arrhythmias. Additional common features in both cases included: fatty metamorphosis and degenerative changes of the approaches to the SA node, the atrial preferential fibers, and the approaches to the AV node, a small AV node, degenerative changes of the bundle branches, and floppy AV valves. These findings show that the pathological substrate of familial supraventricular arrhythmias consists of a diffuse involvement of the entire conduction system, bearing resemblance to pathological findings in elderly subjects with acquired sick sinus syndrome.

Cardiac alternans: diverse mechanisms and clinical manifestations.

OBJECTIVES: The purpose of this review is to assemble the widely dispersed information about cardiac alternans and to categorize the types and mechanisms of alternans, their clinical manifestations and possible therapeutic implications. BACKGROUND: The phenomena of mechanical and electrical alternans have been of continuing interest to both physiologists and clinicians. Recent studies have enhanced this interest because of the reported association of alternans with experimental myocardial ischemia and cardiac arrhythmias. METHODS: The review formulates concepts based on extensive review of published studies and personal observations. RESULTS: Cardiac alternans has been subdivided into the following four categories: 1) mechanical, 2) electrical, 3) in association with myocardial ischemia, and 4) in association with cardiac motion. Mechanical alternans can be explained by hemodynamic or inotropic alterations, or both. Mechanical alternans in the ventricular muscle is accompanied by alternans of action potential shape. In the Purkinje fibers, action potential duration alternates without change in shape and is determined by the duration of the preceding diastolic interval. However, in ventricular muscle fiber, alternans can occur in the presence of constant diastolic intervals. T wave alternans reflects changes in action potential duration and is frequently associated with a long QT interval. Electrocardiographic manifestations of conduction alternans occur at many different sites within the conducting system and myocardium. During myocardial ischemia, additional mechanisms of repolarization alternans have been proposed. Alternans occurring in the presence of a large pericardial effusion is attributed to swinging motion of the heart maintaining two-beat periodicity. CONCLUSIONS: Since its origin as "pulsus alternans" described by Traube in 1872, the definition of alternans has evolved into a term encompassing multiple physiologic and pathologic phenomena that, although united by the term cardiac alternans, diverge widely with respect to etiology, mechanism and clinical significance.