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Myocardial Adaptation, Aging and Failure
Terms in this set (26)
T/F: Myocardial adaptation may be physiologic or pathologic.
Physiologic hypertrophy of the heart can be in response to __. Characterized by ___.
Chronic endurance and strength exercises, pregnancy; Preserves and enhances cardiac function; Characterized by: Increase in thickness of wall and volume of LV (dependent on type of exercise), Increased size of myocardial cells, Capable of regression
T/F: Myocardial cells do not divide.
False. RARELY divide, but sometimes does happen (may be pathologic hypertrophy)
Load against which heart contracts to eject blood; maximum tension of mm mass at end of systole. Experience hypertension, valvular stenosis, increased cardiac mass, sarcomere width is greater than length (W>L),
, little or no change in chamber volume.
Maximum volume of blood at end of diastole; Experience valvular regurgitation, regional dysfunction after MI, dilated cardiomyopathy, increased cardiac mass with increased chamber volume, sarcomere length greater than width (L>W),
Hypertension, valvular stenosis, increased cardiac mass, sarcomere width is greater than length (W>L),
, little or no change in chamber volume. Preload/Afterload Overload?
Experience valvular regurgitation, regional dysfunction after MI, dilated cardiomyopathy, increased cardiac mass with increased chamber volume, sarcomere length greater than width (L>W),
T/F: Concentric hypertrophy can progress into eccentric hypertrophy.
Histologically, what is seen in pathologic hypertrophy?
Increased size of myocardial cells (increased numbers of sarcomeres); Increased nuclear size with
; No significant increase in capillaries, resulting in relative ischemia; Interstitial fibrosis
Excess collagen diffusely infiltrating myocardial wall is indicative of what?
Hypertrophy of the heart
What are some of the biochemical changes in myocardial hypertrophy?
Increased mRNA, increased protein synth, induction of immediate early genes (c-fos, c-myc, EGR-1/Early Growth Response Protein-1, c-jun). Also see re-expression of fetal gene program (
ANP, fetal myosin
), Recapitulation of fetal metabolic program (glycolysis), reorganization of sarcomeres, altered Ca2+ homeostasis, changes in myocyte contractility/relaxation, death of myocytes from apoptosis/replaced by fibrosis, electrical remodeling (alterations in expression/function of ion transporting proteins)
T/F: Arrhythmias are much more common in patients with cardiac hypertrophy.
Increased levels of IGF-1 and IFG-R results in activation of signal transduction pathways, including _____. This is (physiologic/pathologic).
Pathologic hypertrophy is mediated primarily by what types of receptors?
*G-protein coupled receptors, unlike physiologic hypertrophy.
What three transcription factors are activated by signal transduction pathways in myocardial hypertrophy? What do they result in?
GATA4, NFAT, MEF2. They result in increased size of cells by induction of embryonic/fetal genes, increased synth of contractile proteins, and increased production of growth factors (autocrine--act on the cell that produces them)
T/F: Hypertrophy is a reversible phenomenon in the heart.
TRUE. Can suppress pro-growth pathways, activate protein degradative pathways, or go through the ubiquitin proteosome system.
What are some of the most important underlying causes of Left sided cardiac failure?
Ischemic heart disease; systemic hypertension; aortic and mitral valve disease; primary myocardial disease (aka cardiomyopathy)
Extravasation of RBCs in L-sided cardiac failure can result in:
Phagocytosis of RBCs with accumulation of iron (
) in macrophages (heart failure cells)
I am an iron-containing macrophage that you can see when my host coughed up sputum. What am I?
Heart Failure Cells
What is the most common cause of Right-sided cardiac failure?
Left sided failure! ALSO cor pulmonale
(lung disorders like: parenchymal disease of lung, COPD, disorders of pulmonary vasculatory e.g. primary pulmonary hypertension, thrombo-emboli...)
What are some key histological features of R-sided cardiac failure?
Hypertrophy and dilatation of RV, myocyte hypertrophy with variable interstitial fibrosis, dilatation of RA, pericardial effusion
How does right-sided cardiac failure affect organs other than the heart?
Passive congestion of liver with variable centrilobular necrosis (
) with possible progression to cardiac sclerosis; Congestive splenomegaly; Pleural, pericardial, peritoneal (ascites) effusions, peripheral edema
What do I have?
Right-sided cardiac failure
What are some aging changes of the myocardium?
Increased mass (decreased myocytes, increased myocyte size, increased fibrocytes, increased LV stiffness/decreased compliance); Increased subepicardial fat; Accumulation of lipofucsin (aging) pigment; Basophilic degeneration;
Amyloid deposition (Transthyretin)
; Increased LA cavity size, decreased LV cavity size, sigmoid shaped ventricular septum; Aortic valve calcification, mitral annulus calcification, fibrous thickening of leaflets,
; Increased tortuosity and cross sectional diameters of coronary vessels, plaques; dilated ascending aorta, fragmentation of elastica and plaque formation
Brown Atrophy of the Heart
Extensive accumulation of lipofuscin pigment; Atrophy of myocardium; Present in elderly patients, particularly those with cachexia
Congo Red stain is a specific stain for ___. How does it relate to the heart?
Helpful to detect in the aging heart.
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