ABSTRACT
OBJECTIVES: This study aimed to determine the association of stage B heart failure (SBHF) and its constituent left ventricular (LV) abnormalities with trajectory of exercise capacity over time, and assess whether this association is modified by reversion of these LV abnormalities to normal. BACKGROUND: The LV abnormalities of SBHF may coincide with a reduction in exercise capacity that precedes the overt exercise intolerance of clinical heart failure (HF). Determining the predictive capacity of established and novel SBHF criteria for exercise capacity decline may improve HF risk stratification. METHODS: LV structure/function (echocardiography) and exercise capacity (6-min walk distance [6MWD]) were assessed at baseline and 3-year follow-up in 268 patients from the NIL-CHF (Nurse-led Intervention for Less Chronic Heart Failure) study (all stage A [SAHF] or SBHF). Changes (Δ) in 6MWD were compared between SAHF and SBHF and across each of 4 constituent components of SBHF: LV hypertrophy, regional wall motion abnormality(ies) (RWMA), left ventricular systolic dysfunction (LVSD) (ejection fraction <45%) and elevated early diastolic filling/annular velocity ratio (E/e' ≥15). RESULTS: Δ6MWD was similar in those with SAHF (n = 141) and SBHF (n = 127; -5 m [95% confidence interval (CI): -21 to +11 m]; covariate-adjusted). However, within the setting of SBHF there was substantive heterogeneity; that is, reductions in 6MWD were observed with persistent elevated E/e' (-34 m [95% CI: -62 to -6 m]) and persistent LVSD (-41 m [95% CI: -74 to -8 m]), but not with LV hypertrophy (+17 m [95% CI: -15 to +49 m) or RWMA (+5 m [-27 to +36 m]), nor in patients whose elevated E/e' or LVSD reverted to normal by 3 years (p > 0.10). CONCLUSIONS: Elevated E/e' is associated with a similar degree of exercise capacity decline to LVSD, supporting that both LV functional criteria be considered in distinguishing SBHF from SAHF. That reversion of either manifestation of LV dysfunction was associated with preserved exercise capacity advocates targeting of these factors by HF preventive interventions.
Subject(s)
Echocardiography, Doppler, Pulsed , Exercise Tolerance , Heart Failure/diagnostic imaging , Hypertrophy, Left Ventricular/diagnostic imaging , Ventricular Dysfunction, Left/diagnostic imaging , Ventricular Function, Left , Walk Test , Aged , Asymptomatic Diseases , Diastole , Female , Heart Failure/nursing , Heart Failure/physiopathology , Humans , Hypertrophy, Left Ventricular/nursing , Hypertrophy, Left Ventricular/physiopathology , Male , Middle Aged , Severity of Illness Index , Stroke Volume , Systole , Time Factors , Ventricular Dysfunction, Left/nursing , Ventricular Dysfunction, Left/physiopathology , VictoriaABSTRACT
Left ventricular hypertrophy (LVH) is an important independent risk factor for cardiovascular morbidity and mortality. Initially LVH improves contractility and pump function; however, over time a sequence of events occurs including disintegration of myofibrils, interstitial fibrosis, adenosine triphosphate depletion, and altered gene expression. Eventually the hypertrophied myocardium outgrows its capillary bed, subendocardial ischemia develops, and the heart fails. Hemodynamic (pressure) and nonhemodynamic signals (catecholamines, angiotensin II, thyroid hormone) have been identified that stimulate hypertrophic growth of the myocardium. Evidence is also accumulating that the induction of immediate early genes such as c-fos and c-myc may participate in the development of LVH.