PubMed · 7956772
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S Herzig, T Beyer. 1994-10-28. [Sotalol].. https://doi.org/10.1055/s-0029-1235112
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The congenital long-QT syndrome (LQT3) and the Brugada syndrome are distinct, life-threatening rhythm disorders linked to autosomal dominant mutations in SCN5A, the gene encoding the human cardiac Na(+) channel. It is believed that these two syndromes result from opposite molecular effects: LQT3 mutations induce a gain of function, whereas Brugada syndrome mutations reduce Na(+) channel function. Paradoxically, an inherited C-terminal SCN5A mutation causes affected individuals to manifest electrocardiographic features of both syndromes: QT-interval prolongation (LQT3) at slow heart rates and distinctive ST-segment elevations (Brugada syndrome) with exercise. In the present study, we show that the insertion of the amino acid 1795insD has opposite effects on two distinct kinetic components of Na(+) channel gating (fast and slow inactivation) that render unique, simultaneous effects on cardiac excitability. The mutation disrupts fast inactivation, causing sustained Na(+) current throughout the action potential plateau and prolonging cardiac repolarization at slow heart rates. At the same time, 1795insD augments slow inactivation, delaying recovery of Na(+) channel availability between stimuli and reducing the Na(+) current at rapid heart rates. Our findings reveal a novel molecular mechanism for the Brugada syndrome and identify a new dual mechanism whereby single SCN5A mutations may evoke multiple cardiac arrhythmia syndromes by influencing diverse components of Na(+) channel gating function. The full text of this article is available at http://www.circresaha.org.
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The prevalence of panic disorder in patients who present with chest pain or palpitations to a First Heart Aid setting varies in the literature between 0%-59%. In a high percentage of cases, panic disorder is not recognized by the cardiologist in patients who present initially with chest pain or palpitations. Patients with panic disorder have a large and ongoing medical consumption. A selective serotonin reuptake inhibitor and/or cognitive therapy appear to be good treatment of panic disorder in patients who present initially with chest pain or palpitations. A CO2 challenge test elicits the symptoms in patients with panic disorder with high sensitivity and specificity but this test has not been validated in patients who present initially with chest pain or palpitations and in whom the diagnosis 'panic disorder' is not yet established.