Abstract-The trifascicular nature of the intraventricular conduction system and the concept of trifascicular block and hemiblock were described by Rosenbaum and his coworkers in 1968. Since then, anatomic, pathological, electrophysiological, and clinical studies have confirmed the original description and scarce advances have been developed on the subject. In the present study, we attempt to review and redefine reliable criteria for the electrocardiographic and vectorcardiographic diagnosis of left anterior and posterior hemiblock. One of the most important problems related to hemiblocks is that they may simulate or conceal the electrocardiographic signs of myocardial infarction or myocardial ischemia and may mask or simulate ventricular hypertrophy. Illustrative examples of these associations are shown to help the interpretation of electrocardiograms. The incidence and prevalence of the hemiblocks is presented based on studies performed in hospital patients and general populations. One of the most common causes of hemiblocks is coronary artery disease, and there is a particularly frequent association between anteroseptal myocardial infarction and left anterior hemiblock. The second most important cause is arterial hypertension, followed by cardiomyopathies and Lev and Lenègre diseases. The hemiblocks may also occur in aortic heart disease and congenital cardiopathies. Left anterior hemiblock is more common in men and increases in frequency with advancing age. Evidence is presented regarding the relationship of spontaneous closure of ventricular septal defects, which may explain the finding of this and other conduction defects in young populations. Isolated left anterior hemiblock is a relatively frequent finding in subjects devoid of evidence of structural heart disease. Conversely, isolated left posterior hemiblock is a very rare finding; its prognostic significance is unknown and is commonly associated with right bundle-branch block. The most remarkable feature of this association is that the prognosis is much more serious with a great propensity to develop complete atrioventricular block and Adams-Stoke seizures. Key Words: epidemiology Ⅲ heart septal defects Ⅲ myocardial infarction Ⅲ heart block Ⅲ bundle-branch block T hirty-eight years have elapsed since Rosenbaum et al published their seminal work that put together diverse previous observations and brought about a rational and complete analytic approach to the trifascicular concept of intraventricular conduction.These conclusive studies and an exhaustive review of the preceding knowledge of the subject were first published in the Spanish monograph, 1 and later a shorter updated version was presented to acquaint the English reader with the electrocardiographic manifestations and clinical correlation of the abnormal spread of ventricular excitation. 2 A series of articles published by the same authors between 1969 and 1973 also contributed to the expansion of the recognition of this research work. As stated by Herman N. Uhley, 3 this work triggered and infl...
COVID-19 infection has shown rapid growth worldwide, and different therapies have been proposed for treatment, in particular, the combination of immune response modulating drugs such as chloroquine and hydroxychloroquine (antimalarials) alone or in combination with azithromycin. Although the clinical evidence supporting their use is scarce, the off label use of these drugs has spread very quickly in face of the progression of the epidemic and the high mortality rate in susceptible populations. However, these medications can pathologically prolong the QT interval and lead to malignant ventricular arrhythmias such that organized guidance on QT evaluation and management strategies are important to reduce morbidity associated with the potential large-scale use.
The extreme prolongation of ventricular action potential duration that occurs in some of the long QT syndromes may result in two forms of alternating activity of the heart: a "pseudo" 2:1 atrioventricular (AV) block and a T wave alternation, both of which are rate dependent. The pseudo 2:1 AV block relates to the extreme prolongation of ventricular refractoriness. The T wave alternation reflects the fact that the rate dependence of action potential duration differs in degree or magnitude in the subendocardial and subepicardial layers of the ventricular wall. Examples of two cases previously reported in the Journal by Weintraub et al. are used to illustrate and discuss these manifestations.
SUMMARY We studied 12 patients with ventricular parasystole in whom pacemaker activity could be modulated by nonparasystolic beats (NPBs). In six patients (group 1) in whom the intrinsic parasystolic cycle length (XX interval) was obtained without interposed NPBs, we found that NPBs falling during the first half of the cycle prolonged the XRX interval (containing one NPB) and that NPBs falling during the second half of the cycle abbreviated the XRX interval; both effects were maximal when NPBs fell close to the middle of the cycle and were separated by a reversal point. However, because of mutual interference between parasystolic beats and NPBs, only 13.2-43.4% of the parasystolic cycle could be effectively scanned. We also found that the XRX and RX intervals were linearly related. This relationship served to establish that in six patients in whom the XX interval was not obtained (group 2), modulation showed a similar behavior, although neither the reversal point nor the sense of the modulation could be determined. In this report, we suggest diagnostic criteria of parasystolic modulation.IN CLASSIC parasystole, an automatic focus is assumed to be totally independent of the electric activity elsewhere in the heart. Entrance block (a form of unidirectional block) is the barrier that protects the parasystolic center from exogenous influences. However, a mechanism by which nonparasystolic beats (NPBs) can modify the activity of a protected automatic center has been conceived by Jalife and Moe.I They reasoned that "if an impulse cannot invade the pacemaker, but the pacemaker impulses can escape, then clearly there must be a viable ionic pathway across the blocked region." Using an in vitro preparation -the sucrose gap model -they established the existence of an electrotonic action exerted, by evoked action potentials or current pulses, on the activity of a protected pacemak-
The relationship between unstable angor (angina) and circadian periodicity of heart rate variability (HRV) was explored in a group of patients hospitalized in a coronary care unit (CCU). Patients were classified as normal (whose symptoms had non-cardiovascular origin, n=8), moderate angor (n=13) and severe angor (n=11). A fourth group of ambulatory healthy volunteers (n=12) was included. Individual 24 h Holter records were analyzed, mean RR and standard deviation of RR (SDNN) being obtained from 1 h-length windows. For frequency domain analysis, 5 min-length windows were employed. The spectral components analyzed were total power (spectral power between 0.01 and 0.5 Hz), low frequency power (LF: power between 0.04 and 0.15 Hz), and high frequency power (HF: power between 0.15 and 0.4 Hz). In addition, LF to HF areas ratio (L/H) was computed. Mesor, amplitude and acrophase for every 24 h rhythm were calculated by cosinor analysis. As compared to ambulatory controls, admission to the CCU diminished amplitude and phase-delayed the circadian oscillation of most HRV parameters, except for SDNN. Moderate angor patients showed decreased amplitude of RR and L/H and augmented amplitude of SDNN when compared to normal hospitalized subjects. A phase delay of about 1.5 h for RR intervals and a phase advance of 3.5-6 h for LFA and SDNN were found in the moderate angor group when compared to normal. Amplitude of 24 h variation of total power decreased in severely angor patients and the circadian oscillation of HF (an indicator of vagal control on the heart) became free running. A phase delay of 2.5 h in SDNN acrophase was found in severely affected patients when compared to moderate. The results indicate that severity of unstable angor correlates with desynchronization of parasympathetic control of heart rate.
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