PubMed · 6671607
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N Maor, S Keidar, A Palant. 1983-10-02. [Sinus node dysfunction in acute myocardial infarction].. https://pubmed.ncbi.nlm.nih.gov/6671607/
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Patients with congenital heart disease have an increased chance to suffer from brady- as well as tachyarrhythmias. The impact of these on quality of life, morbidity and mortality is more often imperative as compared to heart-healthy individuals. The substrate for these may be either congenital or acquired. Improvements of the surgical management of these patients have led, on the one hand, to improved survival rates with prolonged life expectancy within the last 2 decades, which on the other hand provided the basis for a higher rate of acquired cardiac arrhythmias. Together, this not only challenges diagnostics and therapy but also the prognostic relevance of these arrhythmias. The therapeutic strategies and prognostic markers have until now mostly been based on retrospective studies limited by the low number of patients and inhomogeneous patient selection. Despite these limitations, an increased risk of sudden cardiac death has been substantiated for certain patient groups, e.g., those operated on by the Mustard- or Senning procedures in patients with transposition of the great arteries and patients operated on with correction of the tetralogy of Fallot. However, until now it has not been possible to identify reliable markers for establishing the risk on an individual basis within these patient cohorts. For achieving reliable data on the symptomatic and prognostic effects of present-day--as well as new-coming--therapeutic strategies, it is mandatory to perform prospectively based, randomized multicenter studies. Furthermore, the well-appreciated synergism of hemodynamically and primarily of arrhythmia-based effects on prognosis could potentially be divided into their relative weight to better guide appropriate, substrate-related therapy. In addition, this should help to get better estimates of the risk for sudden cardiac death in different, etiologically homogeneous, groups of patients with congenital heart disease.
The influence of sleep state (i.e., active and quiet) on heart period, heart period variability, respiratory sinus arrhythmia (RSA), and the coupling between RSA and heart period was evaluated in 24 healthy full-term newborns. Electrocardiogram (ECG) data were collected, and sleep state was coded 1 hr after feeding until at least 10 min of data were collected in states of active and quiet sleep. ECG data were analyzed for the first five continuous minutes of each sleep state. Relative to active sleep, quiet sleep was associated with significantly higher amplitude RSA, lower heart period variability, and longer heart periods. Because RSA amplitude reflects the functional output of vagal pathways originating in the nucleus ambiguus, it was hypothesized that sleep state would influence how these vagal pathways regulate instantaneous changes in heart period. A new method, evaluating the instantaneous coupling of RSA and heart period, demonstrated that coupling was significantly greater during active sleep. The neurophysiological explanation extends the polyvagal theory to include potential cortical-brain stem connections.
A woman with congestive heart failure and reduced left ventricular ejection fraction associated with hyperthyroidism is reported. Congestive heart failure resolved and left ventricular ejection fraction normalized within three weeks of treatment of her hyperthyroidism. The literature on previously reported cases of reversible systolic heart failure associated with hyperthyroidism is reviewed and the possible mechanisms leading to systolic dysfunction and congestive heart failure in thyrotoxicosis are discussed. One such mechanism may be the action of thyroid hormone on altering gene expression in cardiac cells; another could be the chronic tachycardia associated with thyrotoxicosis. Although it is a not a common cause of systolic heart failure, thyrotoxicosis should be considered in the differential diagnosis of cardiomyopathies because it is a potentially reversible cause.