Noxious arousal induces T-wave changes in healthy subjects.

BACKGROUND: Sudden arousal has been associated with sudden cardiac death in individuals with ischemic heart disease, cardiac arrhythmias, and the congenital long QT syndrome. This study aimed to determine the effects of arousal on ventricular repolarization in normal individuals by examining the dynamic QT interval-heart rate relationship and T-wave morphology changes under various "arousal" scenarios. METHODS: Eighteen healthy subjects (6 women and 12 men; median age, 22 years) underwent 4 separate 24-hour electrocardiogram recordings using 2-channel Holter recorders. The protocol contained 5 different arousal events: (1) natural waking (woke naturally, then stood up), (2) morning alarm (woken by alarm in the morning, then stood up); (3) night alarm (woken by alarm during the night, then stood up), (4) morning alarm-remain lying (woken by alarm in the morning but remained supine), and (5) lying to standing (stood up from a supine position during the day). Holter recordings were analyzed using a commercial package for dynamic assessment of the QT/RR relationship. RESULTS: In the 20 minutes after arousal, no changes were seen in overall QT/RR relationship in any of the groups. However, marked T-wave morphology changes, including T-wave inversion, were observed in all the arousal events. Postural changes only accounted for a small proportion of change in T-wave morphology. CONCLUSIONS: In healthy subjects, noxious arousal causes marked changes in the morphology of the T wave. This may reflect abnormal adaptation of repolarization to sudden changes in heart rate and autonomic tone.

Abnormalities of the repolarization characteristics of patients with heart failure progress with symptom severity.

BACKGROUND: Congestive heart failure is a common condition with high mortality. Many of these deaths are sudden and unexpected. Ventricular action potential, surface repolarization (QT interval), and dispersion of repolarization are prolonged in the failing heart, contributing to arrhythmogenesis and sudden death. We studied the relationship between QT and heart rate (RR interval) from ambulatory recordings using a novel method in patients with ischemic heart disease and varying degrees of left-ventricular impairment (IHD) and compared them to healthy subjects (HS). We compare the degree of abnormality with the functional impairment and ejection fraction. METHODS: Using a previously described automated method for continuous estimation of the QT/RR characteristic that incorporates a correction formula for compensation of QT adaptation lag (VERDA, Del Mar Reynolds Medical Ltd., Hertford, UK), we compared recordings from 41 IHD patients with age-matched HS. RESULTS: IHD Patients have prolonged 24-hour mean QTo (461 ms vs 426 ms, P < 0.01), and abnormal rate dependence relative to controls (24-hour mean slope: 0.20 vs 0.14, P < 0.001; J: 0.38 vs 0.28, P < 0.001). There is increased temporal variation in J with respect to HS. These abnormalities of repolarization increase with worsening NYHA class, but do not correlate with ejection fraction. CONCLUSIONS: The use of a universal correction formula to compare dynamic QT data in IHD patients is inappropriate. The observed progressive abnormalities may be responsible for the high incidence of sudden death through promotion of arrhythmias.

Predicting death due to progressive heart failure in patients with mild-to-moderate chronic heart failure.

OBJECTIVES: The aim of this study was to explore the value of noninvasive predictors of death/mode of death in ambulant outpatients with chronic heart failure (HF). BACKGROUND: Mortality in chronic HF remains high, with a significant number of patients dying of progressive disease. Identification of these patients is important. METHODS: We recruited 553 ambulant outpatients age 63 +/- 10 years with symptoms of chronic HF (New York Heart Association functional class, 2.3 +/- 0.5) and objective evidence of left ventricular dysfunction (ejection fraction <45%, cardiothoracic ratio >0.55, or pulmonary edema on chest radiograph). After 2,365 patient-years of follow-up, 201 patients had died, with 76 events due to progressive HF. RESULTS: Independent predictors of all-cause mortality assessed with the Cox proportional hazards model were as follows: a low standard deviation of all normal-to-normal RR intervals (SDNN); lower serum sodium and higher creatinine levels; higher cardiothoracic ratio; nonsustained ventricular tachycardia; higher left ventricular end-systolic diameter; left ventricular hypertrophy; and increasing age. Independent predictors of death specific to progressive HF were SDNN, serum sodium and creatinine levels. The hazard ratio of progressive HF death for a 10% decrease in SDNN was 1.06 (95% confidence interval [CI], 1.01 to 1.12); for a 2 mmol/l decrease in serum sodium, 1.22 (95% CI, 1.08 to 1.38); and for a 10 micromol/l increase in serum creatinine, 1.14 (95% CI, 1.09 to 1.19) (all p < 0.01). CONCLUSIONS: In ambulant outpatients with chronic HF, low serum sodium and SDNN and high serum creatinine identify patients at increased risk of death due to progressive HF.