1. Treatment of Heart Failure in Pulmonary Arterial Hypertension—The Urgency of Getting This Right 
Ragavendra R. Baliga, MD, MBA 
Heart Failure Clinics 
Volume 8, Issue 3, Pages xiii-xix (July 2012)
DOI: /j.hfc
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2. Fig. 1
Effect of arterial contracture on vascular resistance. (A) Normal small muscular artery. (B) The same artery completely relaxed. (C) The same artery after development of contracture. This moderate narrowing, if generalized, would increase pulmonary vascular resistance about 10-fold. There is no hypertrophy of arterial wall, cross-sectional area of media being the same in all four diagrams. (D) The same artery as in (C) completely relaxed, showing how resistance may be lowered despite organic arterial disease.
(From Short DS. The arterial bed of the lung in pulmonary hypertension. Lancet 1957;270(6984):12–5; with permission.)
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3. Fig. 2
Photomicrographs of pulmonary artery histologic lesions seen in cases of clinically unexplained pulmonary hypertension. (A) Medical hypertrophy with intimal proliferation. The vascular lumen is markedly reduced, contributing to the elevated resistance. (B) Eccentric intimal fibrosis. These are believed to be related to local thrombin deposition. (C) Plexiform lesion demonstrating obstruction in the arterial lumen, aneurysmal dilation, and proliferation of anastomosing vascular channels. Hematoxylin and eosin stains. (A) and (B), magnification, ×20; (C) magnification, ×4.
(From Braunwald E, Bonow RO. Braunwald's heart disease: a textbook of cardiovascular medicine. 9th ed. Philadelphia: Saunders; 2011; with permission.)
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4. Fig. 3
Proposed pathogenesis for the development of PPH. Genes implicated in the pathogenesis of PPH are prostacyclin synthase, serotonin transporters, nitric oxide synthase, serine elastases, matrix metalloproteinases (MMPs), voltage-gated potassium (Kv) channels, angiotensin-converting enzyme (ACE), vascular endothelial growth factor (VEGF), carbamoyl phosphate synthase, and plasminogen activator inhibitor type 1 (PAI-1). Endothelin-1 production adds to the vasoconstriction in PPH, but whether this is secondary to changes in the above genes, a result of endothelial dysfunction, or a primary pathogenetic event is not clear. Pulmonary vascular remodeling results from the effects of genetics, modifying genes, and environment.
(From Runo JR, Loyd JE. Primary pulmonary hypertension. Lancet 2003;361(9368):1533–44; with permission.)
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5. Fig. 4
Images of the double helical band model of the adult heart. The initial band shape and fitted volume shown from different points of view. (A) The double helical band. (B) The same band color-coded corresponding to physiologic segments. (C) The same band in different orientation, with labeled active and nonactive material, and the apex of the heart. (D) The fitted volumes for left ventricle (LV) and right ventricle (RV) are labeled on these pictures.
(From Grosberg A, Gharib M. Physiology in phylogeny: modeling of mechanical driving forces in cardiac development. Heart Fail Clin 2008;4(3):247–59; with permission.)
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6. Fig. 5
(A) Anatomy of the right-ventricle overload patient with synthetic fiber orientations. (B) Contraction of the model: end-systole position; colors represent the contraction stress. (C) Pressure-volume loops, demonstrating right ventricle enlargement and regurgitations.
(From Sermesant M, Peyrat JM, Chinchapatnam P, et al. Toward patient-specific myocardial models of the heart. Heart Fail Clin 2008;4(3):289–301; with permission.)
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7. Fig. 6
Contrasting mechanisms of ventricular contraction. The RV is morphologically unique from the LV. It has a crescent-like shape and contracts with a peristaltic bellows-like action from apex to base. (A) The RV can accommodate large variations in venous return while maintaining a normal cardiac output. The bellows-like contraction results in a high ratio of RV volume change to RV free-wall surface area change, which allows it to eject a large volume of blood with little alteration in RV wall stretch. The relatively flat relationship between the right ventricular surface area and volume limits the use of the Frank-Starling mechanism to increase the strike volume. The LV has a spherical shape with a distinctly different multiplanar action of contraction that is more like the wringing of a towel. (B) The helical nature of the myocardial bands allows for a twisting motion to eject and reciprocal untwisting to fill rapidly. The twisting action tends to initiate from the apex and progresses toward the base allowing for forceful ejection of blood against high resistance.
(From Rich S. Right ventricular adaptation and maladaptation in chronic pulmonary arterial hypertension. Cardiol Clin 2012;30(2):257–69; with permission.)
Heart Failure Clinics 2012 8, xiii-xixDOI: ( /j.hfc )
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8. Ragavendra R. Baliga, MD, MBA, Consulting Editor
Heart Failure Clinics 2012 8, xiii-xixDOI: ( /j.hfc )
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9. James B. Young, MD, Consulting Editor
Heart Failure Clinics 2012 8, xiii-xixDOI: ( /j.hfc )
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