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Query: UMLS:C0018801 (
heart failure
)
72,216
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Load-adjusted measures of left ventricle (LV) systolic performance are limited by dependence on LV stiffness and afterload. To our knowledge, no stiffness-adjusted and afterload-adjusted indicator was tested in models of pressure (
POH
) and volume overload hypertrophy (VOH). We hypothesized that wall stress reflects changes in loading, incorporating chamber stiffness and afterload; therefore, stroke volume-to-wall stress ratio more accurately reflects systolic performance. We used rat models of
POH
(ascending aortic banding) and VOH (aorto-cava shunt). Animals underwent echocardiography and pressure-volume analysis at baseline and dobutamine challenge. We achieved extreme bidirectional alterations in LV systolic performance, end-systolic elastance (Ees), passive stiffness, and arterial elastance (Ea). In
POH
with LV dilatation and failure, some load-independent indicators of systolic performance remained elevated compared with controls, while some others failed to decrease with wide variability. In VOH, most, but not all indicators, including LV ejection fraction, were significantly reduced compared with controls, despite hyperdynamic circulation, lack of
heart failure
, and preserved contractile reserve. We related systolic performance to Ees adjusted for Ea and LV passive stiffness in multivariate models. Calculated residual Ees was not reduced in
POH
with
heart failure
and was reduced in VOH, while it positively correlated to dobutamine dose. Conversely, stroke volume-to-wall stress ratio was normal in compensated
POH
, markedly decreased in
POH
with
heart failure
, and, in contrast with LV ejection fraction, normal in VOH. Our results support stroke volume-to-wall stress ratio as a load-adjusted and stiffness-adjusted indicator of systolic function in models of
POH
and VOH.
...
PMID:Stroke volume-to-wall stress ratio as a load-adjusted and stiffness-adjusted indicator of ventricular systolic performance in chronic loading. 2292 2
Nonischemic cardiomyopathy (NICM) resulting from long-standing hypertension, valvular disease, and genetic mutations is a major cause of
heart failure
worldwide. Recent observations suggest that myeloid cells can impact cardiac function, but the role of tissue-intrinsic vs. tissue-extrinsic myeloid cells in NICM remains poorly understood. Here, we show that cardiac resident macrophage proliferation occurs within the first week following pressure overload hypertrophy (
POH
; a model of
heart failure
) and is requisite for the heart's adaptive response. Mechanistically, we identify Kruppel-like factor 4 (KLF4) as a key transcription factor that regulates cardiac resident macrophage proliferation and angiogenic activities. Finally, we show that blood-borne macrophages recruited in late-phase
POH
are detrimental, and that blockade of their infiltration improves myocardial angiogenesis and preserves cardiac function. These observations demonstrate previously unappreciated temporal and spatial roles for resident and nonresident macrophages in the development of
heart failure
.
...
PMID:Distinct roles of resident and nonresident macrophages in nonischemic cardiomyopathy. 2971 58
