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The right ventricle (RV) and pulmonary arterial (PA) tree are inextricably linked, continually transferring energy back and forth in a process known as RV-PA coupling. Healthy organisms maintain this relationship in optimal balance by modulating RV contractility, pulmonary vascular resistance, and compliance to sustain RV-PA coupling through life's many physiologic challenges. Early in states of adaptation to cardiovascular disease—for example, in diastolic heart failure—RV-PA coupling is maintained via a multitude of cellular and mechanical transformations. However, with disease progression, these compensatory mechanisms fail and become maladaptive, leading to the often-fatal state of “uncoupling.” Noninvasive imaging modalities, including echocardiography, magnetic resonance imaging, and computed tomography, allow us deeper insight into the state of coupling for an individual patient, providing for prognostication and potential intervention before uncoupling occurs. In this review, we discuss the physiologic foundations of RV-PA coupling, elaborate on the imaging techniques to qualify and quantify it, and correlate these fundamental principles with clinical scenarios in health and disease. © 2022 American Physiological Society. Compr Physiol12: 3705–3730, 2022. The right ventricle (RV) and pulmonary arterial (PA) tree are mechanically coupled. The RV ejects blood to the PAs, which distend, transmit flow onward to the systemic circulation, and reflect flow back toward the RV.RV end-systolic elastance (Ees) is the ability of the RV to generate forward flow, and PA elastance (Ea) is the sum of forces resisting flow. The ratio of Ees/Ea is a commonly used measure of RV-PA coupling.In pulmonary hypertension (PH), Ea is elevated. The RV initially compensates, increasing Ees. As PH progresses, RV force generation fails, decreasing Ees/Ea. This “uncoupling” portends worsening heart failure and death.Traditionally, measuring RV-PA coupling required invasive procedures. Imaging alternatives include echocardiography, quantifying RV and PA pressures, and cardiac MRI (CMR), evaluating RV structure and function. Computed tomography (CT) and nuclear imaging classify etiologies of PH.Mathematical and mechanical models of RV-PA coupling unite physiologic measurements and structural imaging.

The aim of this study was to define the population-based familial clustering of atrial fibrillation (AF) that is associated with fibrosis and describe evidence for a heritable predisposition.

The ratio of right ventricular end-diastolic diameter (EDD) to left ventricular EDD (RV/LV) is a measure predictive of right ventricular failure. We hypothesized that an increase in RV/LV would be associated with poor prognosis in severe sepsis and septic shock.

This study retrospectively evaluated the feasibility and esophageal thermal injury (ETI) patterns of high-power short-duration (HPSD) radiofrequency atrial fibrillation (AF) ablation.

Your 'Rich Son. Poor Son' Publisher's Note in the (April 2006) issue of Hawaii Business is right on!!! So many people forget the importance of the intangible gifts we receive [...]

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Agouti protein and Agouti-related protein (Agrp) are paracrine signaling molecules that act by antagonizing the effects of melanocortins, and several alternatives have been proposed to explain their mechanisms of action. Genetic crosses in a sensitized background uncover a phenotypic difference between overexpression of Agoutiand loss of Mc1r function, demonstrate that a functional Mc1r is required for the pigmentary effects of Agouti, and suggest that Agouti protein can act as an agonist of the Mc1r in a way that differs from ?-MSH stimulation. In vitro, Agouti protein inhibits melanocortin action by two mechanisms: competitive antagonism that depends on the carboxy-terminus of the protein, and downregulation of melanocortin receptor signaling that depends on the aminoterminus. Our findings provide evidence of a novel signaling mechanism whereby ?-MSH and Agouti protein function as independent ligands that inhibit each other's binding and transduce opposite signals through a single receptor.

Increasing evidence suggests that the formation of oxidized low‐density lipoprotein (Ox‐LDL) in vivo is associated with the development of atherosclerotic vascular disease. We investigated the effects of Ox‐LDL on two vascular endothelial cell coagulant properties, tissue factor expression, and protein C activation. The Ox‐LDL increased human arterial and venous endothelial cell tissue factor activity, with 100 μg/ml of Ox‐LDL increasing tissue factor activity fourfold. Native LDL modified by incubation with cultured human arterial and venous endothelial cells also induced endothelial cell tissue factor activity. This modification was blocked by coincubation with the antioxidants, probucol or ascorbic acid. It was determined, based on inhibition by known scavenger receptor antagonists (fucoidin, dextran sulfate), that binding of Ox‐LDL via the acetyl LDL (scavenger) receptor was partially responsible for the increase in tissue factor expression. Whereas endothelial cell tissue factor expression was increased by incubation with Ox‐LDL, protein C activation was reduced ~ 80% by incubating cultured endothelial cells with Ox‐LDL. The effect of Ox‐LDL on protein C activation was not inhibited by antagonists to the scavenger receptor. These data indicating that an atherogenic lipoprotein can regulate key vascular coagulant activities provide an additional link between vascular disease and thrombosis.—Weis, J. R.; Pitas, R. E.; Wilson, B. D.; Rodgers, G. M. Oxidized low‐density lipoprotein increases cultured human endothelial cell tissue factor activity and reduces protein C activation. FASEB J.5: 2459–2465; 1991.

Several letters to the editor are presented in response to previous articles, including "Rich Son, Poor Son," in the April 2006 issue, another about worrisome economic trends that people should be aware of, in the March 2006 issue, and "Pooling Together: A Health Insurance Pool May Help Hawaii's Small Businesses," in the April 2006.