PubMed · 14272428
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G N WEBB. 1965. THE CONTOUROGRAM.. https://pubmed.ncbi.nlm.nih.gov/14272428/
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Depressed heart rate variability (HRV) is a powerful independent predictor of a poor outcome in patients with chronic and stable congestive heart failure (CHF). However, the prognostic value of HRV analysis in patients hospitalized for decompensated CHF is not known. The aim of this study was to investigate whether HRV parameters obtained during admission for decompensated CHF could predict survival after hospital discharge. We studied 199 patients (131 men, aged 60 +/- 14 years) with a previous diagnosis of New York Heart Association class III or IV CHF who were admitted to the hospital for decompensated CHF. Twenty-four-hour Holter recordings were obtained on admission, and measures of HRV were calculated in the time and frequency domain. During a mean follow-up of 312 +/- 150 days, 40 patients (21.1%) died. Kaplan-Meier analysis indicated that patients with SD of the RR intervals over a 24-hour period (p = 0.027), SD of all 5-minute mean RR intervals (p = 0.043), total power (p = 0.022), and ultra-low-frequency power (p = 0.008) in the lower tertile were at a higher risk of death. In a multivariate Cox regression model, the same indexes in the lower tertile were independent predictors of mortality: SD of the RR intervals over a 24-hour period (risk ratio [RR] 2.2, 95% confidence interval [CI] 1.05 to 4.3, p = 0.036), SD of all 5-minute mean RR intervals (RR 2.1, 95% CI 1.05 to 4.2, p = 0.04), total power (RR 2.2, 95% CI 1.08 to 4.2, p = 0.03), and ultra-low-frequency power (RR 2.6, 95% CI 1.3 to 5.3, p = 0.007). Therefore, the severity of autonomic perturbations during hospital admission for CHF decompensation, as reflected by measures of overall HRV, can predict survival after hospital discharge. Together with previous studies, our findings suggest that indexes of overall HRV provide useful prognostic information in the full spectrum of CHF severity.
AIMS: The prognostic value of admission troponin T (tnT) levels and the resolution of the ST-segment elevation in ST-elevation myocardial infarction (STEMI) is well established. However, the combination of these two early available markers for predicting risk has not been evaluated. METHODS AND RESULTS: We evaluated 516 patients with fibrinolytic treated STEMI from the ASSENT-2 and ASSENT-PLUS studies, which had both admission tnT and ST-monitoring available. We used a prospectively defined cut-off value of tnT of 0.1microg/l. For ST-segment resolution, a cut-off of 50% measured after 60min was used. Both a tnT >/=0.1microg/l (n=116) and ST-segment resolution <50% (n=301) were related to higher one-year mortality, 13% vs 4% (P<0.001) and 8.4% vs 2.8% (P=0.009), respectively. In a multivariate analysis ST-segment resolution was and tnT showed a strong trend to be independently related to mortality. The combination of both further improved risk stratification. The one-year mortality in the group with elevation of tnT and without ST-segment resolution compared to the group without tnT elevation and with ST-segment resolution was 18.2% vs 2.8% (P<0.001). CONCLUSIONS: Both tnT on admission and ST-segment resolution after 60min are strong predictors of one-year mortality. The combination of both gives additive early information about prognosis and further improves risk stratification.
Voltage-gated sodium channels are transmembrane proteins that produce the ionic current responsible for the rising phase of the cardiac action potential and play a fundamental role in the initiation, propagation, and maintenance of normal cardiac rhythm. Inherited mutations in SCN5A, the gene encoding the pore-forming subunit of the cardiac Na+ channel, have been associated with distinct cardiac rhythm syndromes: the congenital long QT syndrome, Brugada syndrome, and isolated conduction disease. Electrophysiologic characterization of heterologously expressed mutant Na+ channels have revealed gating defects that, in many cases, can explain the distinct phenotype associated with the rhythm disorder. However, recent studies have revealed significant overlap between aberrant rhythm phenotypes, and single mutations have been identified that evoke multiple rhythm disorders with common gating lesions. These new insights enhance understanding of the structure-function relationships of voltage-gated Na+ channels, and also highlight the complexities involved in linking single mutations, ion-channel behavior, and cardiac rhythm.